Antioxidant effects of piperine in in-vivo chick embryo cataract model induced by steroids

Purpose: The etiopathogenesis of steroid-induced cataracts is unknown. One hypothesis is that the higher reactive oxygen species (ROS) levels play an important role in the pathogenesis of several disorders, including the evolution of cataracts. This study investigated the antioxidant effects of piperine in our steroid-induced chick embryo lens model.

Methods: The study included 36 specific pathogen-free (SPF) fertilized eggs divided into six groups: phosphate buffer saline (PBS, pH 7.4 Saline Solution (0.9%) isotonic) group (G1), hydrocortisone succinate sodium (HC)-treated group (G2), 100?mg/kg piperine and HC treated group (G3), 50?mg/kg piperine and HC treated group (G4), 25?mg/kg piperine and HC treated group (G5), and 10?mg/kg piperine and HC treated group (G6). On the 15th day of incubation, the SPF eggs in the six groups were removed from the incubator; all were injected using insulin injectors into the chorioallantoic membrane. On day 17, all of the chick embryos were removed from the eggs and all lenses were dissected from the embryos. Cataract formation was evaluated in all lenses, and total antioxidant status (TAS), total oxidant status (TOS), reduced glutathione (GSH), and lipid peroxidation (MDA, malondialdehyde) levels were measured in all lens.

Results: The lenses in the G1 group had higher levels of GSH and TAS (p?p?p?p?p?p?p?Conclusion: Steroid therapy causes a decrease in GSH and TAS levels and an increase in TOS and MDA levels in lens tissues, indicating increased oxidative stress. Piperine exerts its effects as an antioxidant substance, in increasing doses.     

Antioxidant activity of olive wine,a byproduct of olive mill wastewater

Context Although olive mill wastewater (OMWW) is a good source of bioactive phenolic compounds, disposing OMWW is a serious environmental challenge. Production of wine via fermenting OMWW may be a promising alternative to deal with OMWW. However, whether or not olive wine from OMWW still reserves its original bioactivities remains unclear.

Objective This study examines antioxidant activity of olive wine fermented from OMWW.

Materials and methods Hydroxytyrosol in olive oil was determined by HPLC. Total flavonoid, total polyphenol and in vitro antioxidant activities were measured by spectrophotometry. Aged mice were intragastricly administered 7, 14 and 28?mL/kg olive wine consecutively for 30 d. Afterward, levels of malonaldehyde (MDA), protein carbonyl, reduced glutathione (GSH) and activity of superoxide dismutase (SOD) were assayed in mouse plasma and liver.

Results Contents of hydroxytyrosol, total flavonoid and total polyphenol in olive wine were 0.14?±?0.01, 0.29?±?0.06 and 0.43?±?0.03?mg/mL, respectively. The IC₅₀ value of olive wine to scavenge DPPH and hydroxyl free radicals was 2.5% and 3.2% (v/v), respectively. Compared with the solvent control group, olive wine with a dose of 28?mL/kg remarkably lowered mouse MDA concentration in liver, and reduced protein carbonyl level in plasma (p?<?0.05). Meanwhile, olive wine at doses of 7 and 28?mL/kg notably enhanced SOD activity in both mouse plasma and liver (p?<?0.05). The beneficial effect on liver was superior to that of γ-tocopherol.

Conclusion The study demonstrated that olive wine from OMWW has potential for treating oxidative stress-associated diseases.     

Effects of Pycnogenol on cisplatin-induced optic nerve injury: an experimental study

Aim: To determine the effects of Pycnogenol on cisplatin-induced optic nerve damage.

Material and method: Totally 18 albino Wistar male rats were assigned into three groups, with six rats in each group as follows: healthy controls (HC group), only cisplatin (2.5?mg/kg) administered group (CIS group) and Pycnogenol (40?mg/kg)?+?cisplatin (2.5?mg/kg) administered group (PYC group). We analyzed the levels of malondialdehyde (MDA) as a marker of lipid peroxidation and oxidative stress, total glutathione (tGSH) as a marker of antioxidant status, nuclear factor-kappa B (NF-κB) and tumor necrosis factor alpha (TNF-α) as inflammatory markers, total oxidative status (TOS) and total antioxidant status (TAS) on eye tissue together with histopathological evaluation of optic nerve in an experimental model.

Results: In CIS group MDA, TOS, TNF-α and NF-κB levels were statistically significantly higher (p?p?p?p?Conclusion: Pycnogenol pretreatment was highly effective in preventing augmentation of cisplatin-induced oxidative stress and inflammation in eye tissue.     

The effects of lycopene on alloxan induced diabetic optic neuropathy

Aim: To determine the effects of lycopene treatment in prevention of diabetes associated inflammatory response and oxidative stress in an experimental model. With this aim we investigated the levels of oxidative stress markers including Malondialdehyde (MDA), and total oxidative status (TOS)together with inflammatory markers including nuclear factor- kappa B (NFKB) and tumor necrosis factor α (TNF-α) and antioxidants including total glutathione (TGSH), total oxidative status (TOS) and total anti-oxidative status (TAS) levels on eye tissue.

Material and methods: Totally 18 albino Wistar male rats (250–280 grams) assigned into three groups, with six rats in each group as follows: healthy group (HG), control group (CG), and lycopene group (LG). The diabetes was induced with alloxan administration in rats of CG and LG. Lycopene (4?mg/kg) was administered to the rats in LG once a day for 3?months. At the end of this period, the animals were sacrificed and their eyes were enucleated for histopathological evaluations. From the tissues, MDA, GSH, TOS, TAS, TNF-α and NF-κB levels were analyzed.

Results: MDA, TOS, OSI, NFKB and TNF-α levels were significantly higher, while TGSH and TAS levels were significantly lower in CG compared with HG (p?p?Conclusion: For the first time in literature we determined that, lycopene was significantly effective in prevention of augmented inflammation and oxidative stress on eye tissue associated with diabetes, as well as the tissue damage on optic nerve. However, studies investigating the long-term clinical effects of lycopene on diabetic individuals are warranted.     

Neuroprotective effects of alkaloids from Piper longum in a MPTP-induced mouse model of Parkinson’s disease

Abstract

Context: Alkaloids of Piper longum L. (Piperaceae) (PLA) include piperine and piperlonguminine. Piper longum and piperine have multiple biological properties including antioxidant activity.

Objective: The present study investigated the neuroprotective effects of PLA in a MPTP-induced mouse model of Parkinson’s disease.

Materials and methods: PLA was prepared by extracting the dry seed of P. longum using 85% ethanol. Adult male C57BL/6 mice were divided into eight groups of 12 rats each. Experimental and control groups received an equivalent volume of saline, 0.5% CMC-Na, and 0.1% Tween 80, treated groups received oral PLA (30, 60, and 120?mg/kg), other groups treated with piperine (60?mg/kg) or Madopar (50?mg/kg). The PLA prevention group (PLA-Pr) administrated PLA (120?mg/kg) for 1 week before MPTP challenged. Except for the PLA-Pr group, others were treated for seven consecutive weeks. Parkinson’s disease was induced by injecting MPTP intraperitoneally (25?mg/kg) twice weekly for five consecutive weeks. Dopaminerigic (DA) neurons and their metabolism were detected by UFLC-MS/MS. Tyrosine hydroxylase (TH)-immunohistochemistry assay and Western blotting were performed. The antioxidant enzymatic levels were determined by kit-based assays.

Results: The LD₅₀ value of PLA was determined at 1509?mg/kg of body weight. PLA (60?mg/kg) can significantly increase total movement time and distance (p?<?0.05), increase levels of DA (p?<?0.05) and DOPAC (p?<?0.05), increase glutathione (GSH) level and superoxide dismutase (SOD) activity (p?<?0.05), and decrease the lipid peroxidation of malondiadehycle (MDA) (p?<?0.05) in PLA-treated groups as compared with the control group.

Discussion and conclusion: Our results indicate that PLA possesses neuroprotective effects and has ameliorative properties in dopaminergic neurons.     

The protective potential of metformin against acetaminophen-induced hepatotoxicity in BALB/C mice

Context: Acetaminophen overdose is regarded to a common cause of acute liver failure. The hepatotoxicity leads to mitochondrial oxidative stress and subsequent necrotic hepatocellular death.

Objective: This study examines the protective effect of metformin on acetaminophen-induced oxidative stress, inflammation and subsequent hepatotoxicity in mice.

Materials and methods: Male BALB/c mice were orally administered to acetaminophen (250?mg/kg/d) for a 7-day period. The mice received metformin (100 and 200?mg/kg/d, p.o.) for 21 days. To evaluate acetaminophen-induced oxidative stress, liver tissue level of malodialdehyde (MDA), end product of membrane lipid peroxidation, and activities of superoxide dismutase (SOD) and glutathione (GSH) were measured. Histological analysis and measurement of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were performed. Moreover, tissue concentrations of proinflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), along with, C-reactive protein (CRP) were assessed.

Results: Acetaminophen caused focal hepatocyte necrosis, inflammation and fatty degeneration, as well as increased tissue levels of AST, ALT, ALP and MDA, and also decreased GSH and SOD activities. Moreover, IL-6, TNF-α and CRP levels were increased following acetaminophen hepatotoxicity. Metformin (200?mg/kg/d) significantly normalized MDA, SOD and GSH levels (p?<?0.001), and exerted a hepatoprotective effect by significant decreasing ALT, AST and ALP concentrations (p?<?0.001). The tissue levels of IL-6, TNF-α and CRP were markedly decreased by 21-day treatment with metformin (200?mg/kg/d) (p?<?0.001).

Discussion: The results suggest metformin protects hepatocytes against acute acetaminophen toxicity. Metformin is indicated to diminish oxidative stress, proinflammatory cytokines, and hepatocyte necrosis.     

Levels of paraoxonase,an index of antioxidant defense,in patients with active sarcoidosis

ABSTRACT

Objective: Oxidative mechanisms are currently discussed as playing a crucial role in the genesis of inflammatory lung diseases. We aimed to evaluate the oxidant–antioxidant balance in the pathogenesis and activity of sarcoidosis and to search if the change in the level of PON can be taken as an activity marker.

Methods: 26 active sarcoidosis subjects aged 41.3?±?12.9 years, 37 inactive subjects aged 39.6?±?11.7 years and 48 control subjects aged 48.9?±?2.5 years were recruited in our study. Malondialdehyde (MDA), paraoxonase1 (PON1) and oxidized low density lipoprotein (oxLDL) levels in serum were analyzed by spectrophotometric, kinetic, and ELISA methods, respectively.

Results: PON1 levels were significantly lower in the active disease state than both the inactive form and control groups. MDA levels were significantly higher in active sarcoidosis than both the inactive disease and control groups, and oxLDL levels were significantly higher in the active disease group than the inactive group and control group. The level of PON1 in the inactive disease group is not significantly different from the control group while the oxLDL and MDA levels of inactive group is significantly higher than the control group (p?<?0.001). There was a negative correlation between the PON1 activities and MDA values in both active and inactive groups (p?=?0.008).

Conclusion: Oxidative stress increases in sarcoidosis might be due to both increase in lipid peroxidation and decrease in antioxidant status (PON1) and the relationship between oxidative status and the activation of the disease should be discussed by comparing the previously known activation criteria.     

Effect of pre- and postnatal exposure to urban air pollution on myocardial lipid peroxidation levels in adult mice

Exposure to air pollution can elicit cardiovascular health effects. Children and unborn fetuses appear to be particularly vulnerable. However, the mechanisms involved in cardiovascular damage are poorly understood. It has been suggested that the oxidative stress generated by air pollution exposure triggers tissue injury. To investigate whether prenatal exposure can enhance oxidative stress in myocardium of adult animals, mice were placed in a clean chamber (CC, filtered urban air) and in a polluted chamber (PC, São Paulo city) during the gestational period and/or for 3?mo after birth, according to 4 protocols: control group—prenatal and postnatal life in CC; prenatal group—prenatal in PC and postnatal life in CC; postnatal group—prenatal in CC and postnatal life in PC; and pre–post group—prenatal and postnatal life in PC. As an indicator of oxidative stress, levels of lipid peroxidation in hearts were measured by malondialdehyde (MDA) quantification and by quantification of the myocardial immunoreactivity for 15-F2t-isoprostane. Ultrastructural studies were performed to detect cellular alterations related to oxidative stress. Concentration of MDA was significantly increased in postnatal (2.45?±?0.84?nmol/mg) and pre–post groups (3.84?±?1.39?nmol/mg) compared to the control group (0.31?±?0.10?nmol/mg) (p?<?.01). MDA values in the pre–post group were significantly increased compared to the prenatal group (0.71?±?0.15?nmol/mg) (p?=?.017). Myocardial isoprostane area fraction in the pre–post group was increased compared to other groups (p?≤?.01). Results show that ambient levels of air pollution elicit cardiac oxidative stress in adult mice, and that gestational exposure may enhance this effect.     

Effects of macamides on endurance capacity and anti-fatigue property in prolonged swimming mice

Context: Lepidium meyenii Walp. (Brassicaceae), most commonly known as “maca”, has been used as a food or folk medicine to improve vitality in Peru. Previous research demonstrated that lipid-soluble extract from maca improved swimming endurance capacity. Macamides are considered the typical lipid-soluble markers for maca and proved to have several pharmacological properties, such as improving sexual performance and neuroprotective activies.

Objective: The present study investigates the effects of macamides on endurance capacity and anti-fatigue property in prolonged swimming mice.

Materials and methods: The Balb/c mice were divided into seven groups: a control group, low-dose groups of N-benzyllinoleamide, N-benzyloleamide, and N-benzylpalmitamide, high-dose groups of these macamides. The macamides groups received the commercial products (12 and 40?mg/kg, ig), while the control group received vehicle for 21 d. On the 14th day, the mice were given the weight-loaded swimming test. On the 21st day, the mice were sacrificed immediately after 90?min swimming, and some biochemical parameters were measured.

Results and discussion: Compared with the control group, exhaustive swimming time was significantly prolonged in high-dose group of N-benzyloleamide (p?<?0.05); the levels of lactic acid (LD), blood ammonia (BA), and lactate dehydrogenase (LDH) were significantly decreased (p?<?0.05), whereas the levels of liver glycogen (LG) and non-esterified fatty acid (NEFA) were significantly increased (p?<?0.05) in high-dose group of N-benzyloleamide. The malondialdehyde (MDA) contents in the brain, muscle, and liver were significantly decreased (p?<?0.05), whereas superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities in the brain, muscle, and liver were significantly increased in high-dose group of N-benzyloleamide (p?<?0.05).

Conclusion: The results indicate that N-benzyloleamide has pharmaceutical property against exercise-induced fatigue, and this effect can be explained by the modulated energy metabolism and improved antioxidant status.     

Improved oral efficacy of epirubicin through polymeric nanoparticles: pharmacodynamic and toxicological investigations

Epirubicin (EPI) elicits poor-oral bioavailability hence commercially available as injection for intravenous administration which follows a rapid increase and fast decay in plasma drug concentration often needs a frequent dosing that may lead to serious side effects. Aim of the present study is to develop a nanoparticulate system which could deliver epirubicin effectively via oral administration and could eventually promote new concept “chemotherapy at home.” In this perspective, epirubicin loaded Poly-lactide-co-glycolic acid nanoparticles (EPI-NPs) were developed by double emulsion evaporation techniques and evaluated for its safety and efficacy against Ehrlich’s Ascites (EAT) induced tumor in balb/c mice. In vivo fate of nanoparticles after oral administration in Albino wistar rats was also studied. EPI-NPs showed marked reduction in tumor size ～40% while tumor size was increased 3.55 and 3.28 folds in control as well as in group treated orally with free epirubicin solution (EPI-S), respectively. Furthermore, toxicological evaluation demonstrated insignificant difference in levels of biomarkers including MDA, CAT, SOD, LDH, CK-MB, AST and ALT when EPI-NPs-oral treatment was compared with control group while levels of these biomarkers were found extremely significant in group treated with EPI-S (i.v). and demonstrated increment in LDH (p?<?0.001), CK-MB (p?<?0.001), AST (p?<?0.001), ALT (p?<?0.001) and MDA levels (p?<?0.001) and reduction in SOD (p?<?0.001) and CAT levels (p?<?0.001) thus confirmed better safety profile of EPI-NPs oral than EPI-S i.v. Biodistribution study demonstrated the presence of NPs in different body organs and blood which suggests probability of NPs translocation across intestine thus at the tumor site.     

Cardioprotective effect of whole fruit extract of pomegranate on doxorubicin-induced toxicity in rat

Context: Cardioprotective effects of various plants are generally attributed to their antioxidant activity. The whole fruit extract of pomegranate (WFEP), Punica granatum L. (Punicaceae), has a potent antioxidant activity.

Objective: To investigate cardioprotective effect of WFEP against doxorubicin (Dox)-induced cardiotoxicity in rats.

Materials and methods: Male Wistar rats were divided randomly into three groups of eight rats each: control (water, 5?mL/kg); Dox (10?mg/kg i.v.) and WFEP (100?mg/kg). Dox was administered in Dox and WFEP groups. After anesthetizing the animals on the last day, electrocardiogram was recorded and blood was analyzed for creatine kinase-MB isoenzyme (CK-MB), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) activities. Determinations of superoxide dismutase (SOD), reduced glutathione (GSH), lipid peroxidation (LPO) and histopathology of the heart tissues were carried out.

Results: The WFEP group showed decreased QT and increase in heart rate (p?<?0.05) compared to the Dox group. Significant decrease in CK-MB (p?<?0.01), LDH (p?<?0.05) and no such significant decrease in AST were observed as compared to the Dox group. There was significant increase in the level of GSH (p?<?0.05), whereas inhibition of LPO and increase in SOD concentration was not significant in the WFEP group compared to the Dox group. Histopathological study of the WFEP-treated group showed slight protection against myocardial toxicity induced by Dox.

Conclusion: Results indicate that WFEP has cardioprotective effect against Dox-induced cardiotoxicity in rats.     

Riboflavin attenuates lipopolysaccharide-induced lung injury in rats

Abstract

Riboflavin (vitamin B2) is an easily absorbed micronutrient with a key role in maintaining health in humans and animals. It is the central component of the cofactors flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) and is therefore required by all flavoproteins. Riboflavin also works as an antioxidant by scavenging free radicals. The present study was designed to evaluate the effects of riboflavin against acute lungs injury induced by the administration of a single intranasal dose (20?μg/rat) of lipopolysaccharides (LPS) in experimental rats. Administration of LPS resulted in marked increase in malondialdehyde (MDA) level (p?<?0.01) and MPO activity (p?<?0.001), whereas marked decrease in glutathione (GSH) content (p?<?0.001), glutathione reductase (GR) (p?<?0.001) and glutathione peroxidase (p?<?0.01) activity. These changes were significantly (p?<?0.001) improved by treatment with riboflavin in a dose-dependent manner (30 and 100?mg/kg, respectively). Riboflavin (100?mg/kg, p.o.) showed similar protective effects as dexamethasone (1?mg/kg, p.o.). Administration of LPS showed marked cellular changes including interstitial edema, hemorrhage, infiltration of PMNs, etc., which were reversed by riboflavin administration. Histopathological examinations showed normal morphological structures of lungs tissue in the control group. These biochemical and histopathological examination were appended with iNOS and CAT gene expression. The iNOS mRNA expression was increased significantly (p?<?0.001) and levels of CAT mRNA expression was decreased significantly (p?<?0.001) in the animals exposed to LPS, while treatment with riboflavin significantly (p?<?0.01) improved expression of both gene. In conclusion, the present study clearly demonstrated that riboflavin caused a protective effect against LPS-induced ALI. These results suggest that riboflavin may be used to protect against toxic effect of LPS in lungs.     

Protective effects of N-acetylcysteine on triamcinolone acetonide-induced lens damage in rats

Objective: To examine the relationship of cataract forming effect of intravitreal triamcinolone acetonide (IVTA) injection with oxidative status and the effect of N-acetylcysteine (NAC) on these alterations.

Materials and methods: Twenty-six Wistar-Albino rats were included in the study. Rats were assigned into four groups as follows: intravitreal saline injection group (controls); IVTA injection group; IVTA?+?intraperitoneal NAC injection group (IVTA?+?NAC); and intraperitoneal NAC injection group (NAC). Triamcinolone acetonide was intravitreally injected at a dose of 1?mg. NAC was intraperitoneally injected at a dose of 150?µg/g body weight. Animals were sacrificed and lens specimens were analyzed for levels of malondialdehyde (MDA) and protein carbonyl (PC) and activities of glutathione (GSH) and glutathione peroxidase (GSH-Px).

Results: We found that the MDA and PC levels of lenses were increased in the IVTA group (p?p?p?Conclusion: These results indicate that the NAC produces a protective mechanism against IVTA-induced cataract and suggest a role of oxidative stress in pathogenesis.     

Efficacy of Aloe vera/olive oil cream versus betamethasone cream for chronic skin lesions following sulfur mustard exposure: a randomized double-blind clinical trial

Background: Chronic pruritic skin lesions are among the common late complications of sulfur mustard intoxication. In the present randomized double-blind clinical trial, therapeutic efficacy of Aloe vera/olive oil combination cream in the alleviation of these lesions was evaluated and compared to that of betamethasone 0.1% cream.

Methods: Sixty-seven Iranian chemical warfare-injured veterans were randomized to apply A. vera/olive oil (n?=?34, completers?=?31) or betamethasone 0.1% (n?=?33, completers?=?32) cream twice daily for 6 weeks. Evaluation of pruritus severity was performed using a pruritic score questionnaire and visual analogue scale (VAS).

Results: Both treatments were associated with significant reductions in the frequency of pruritus (p?<?0.05), burning sensation (p?<?0.01 and p?<?0.001 in A. vera/olive oil and betamethasone group, respectively), scaling (p?<?0.01 and p?<?0.05) and dry skin (p?<?0.001) at the end of trial. Fissure and excoriation were only reduced in the A. vera group (p?<?0.05). The change in the frequency of hyper- and hypopigmentation lesions, blisters, erythema and lichenification did not reach statistical significance in any of the groups (p?>?0.05). Mean pruritus (p?<?0.05) and VAS scores (p?<?0.01 and p?<?0.05) were significantly decreased by the end of trial in both groups. The rate of improvement in the pruritus severity [defined as being classified in a less severe category (mild, moderate and severe)] was found to be comparable between the groups (p?>?0.05).

Conclusion: A. vera/olive oil cream was at least as effective as betamethasone 0.1% in the treatment of sulfur mustard-induced chronic skin complications and might serve as a promising therapeutic option for the alleviation of symptoms in mustard gas-exposed patients.     

Role of innate immunity and oxidative stress in steroid-induced cataracts in developing chick embryos

Purpose: The exact etiopathogenesis of steroid-induced cataracts (SIC) is not known. Although oxidative stress is one of the most acceptable hypotheses, the exact molecular events in steroid-induced oxidative events in the lens need to be clarified. In addition, to the best of our knowledge, the innate immune system components in SIC formation have not been studied previously. The aim of the present study was to study the oxidative system and the innate immune system components in the cataractous lenses of a developing chick embryo SIC model.

Materials and methods: The study included 20 specific pathogen-free (SPF) fertilized eggs divided into two groups, with one hydrocortisone (HC)-treated group (G1) and one non-HC-treated control group (G2). On the 15th day of incubation, the SPF eggs in the two groups were removed from the incubator; HC was injected into G1, and phosphate-buffered saline (PBS) was injected into G2 using insulin injectors into the chorioallantoic membrane. On day 17, all of the chick embryos were removed from the eggs, and all lens and liver tissues were dissected from the embryos. Cataract formation was evaluated in all lenses, and total antioxidant status (TAS), total oxidant status (TOS), reduced glutathione (GSH), oxidized glutathione (GSSG), interleukin-6 (IL-6), and interleukin-1β (IL-1β) levels were measured in all lens and liver tissues.

Results: The lenses in the SIC group had lower levels of GSH, GSSG, TAS, and IL-6 (p?=?0.016, 0.022, 0.000, 0.000, respectively), and higher levels of TOS (p?=?0.000) than the control group. Furthermore, the liver tissues in the SIC group had decreased levels of TAS and IL-6, and increased levels of TOS compared to the control tissues (p?=?0.000). Although the IL-1β levels in the lens and liver tissues in the HC-induced cataract group were lower than in the control group, these differences were not statistically significant. In addition, the GSH levels in the liver tissues did not statistically differ between the two groups despite the significant GSH difference in the lens tissues.

Conclusions: Steroid therapy causes a decrease in GSH, GSSG, and TAS levels and an increase in TOS levels in lens tissues, which means there is increased oxidative stress and decreased antioxidant defence. Furthermore, lenses with SIC have lower IL-6 levels compared to non-cataractous lenses. The interaction between lenticular IL-6 and antioxidant defence needs to be further studied.     

Effect of alpha lipoic acid on smoking-induced skin damage

Objective: Exposed to cigarette leads to the formation of reactive oxygen species and the generation of bioactive molecules that can damage skin cells. This investigation was carried out to study possible effects of Alpha Lipoic Acid (ALA) on smoking-induced rat skin injury.

Materials and methods: 28 Spraque–Dawley female rats were allocated into three groups: control group (n?=?8), smoking group (n?=?10; 12 cigarettes/day, 8 weeks) and smoking?+?ALA group (n?=?10; 12 cigarettes/day?+?100?mg/kg, 8 weeks). Experiment group animals were sacrificed under anaesthesia with 10%ketamine?+?2%xylasine at the end of second mounts and then skin examples were taken from the epigastric area. Histochemical (Haematoxylin–Eosin and Masson’s trichrome, immunohistochemical (TNF-α) and biochemical analysis (CAT, MDA and protein carbonylation) were performed on these skin tissues.

Results: Histologically, skin was distinguished normal structure in the control group. In the smoking group, collagen bundles and hair follicle degradation/reduction, sweat gland degeneration, mononuclear cell infiltration in dermis were encountered. In ALA-treated group, all of these changes were improved (p?<?0.05). Collagen bundles structures were appearance more regular than the smoking group . Immunohistologically, intense staining was observed in the smoking group, while very weak staining was observed in control group, weak staining was observed in the ALA-treated group. Biochemically; The CAT activity compared to cigarette group with control was raised high and in ALA group was higher compared to both groups, but not significant (p?>?0.05). MDA; which is indicator of lipid peroxidation was significantly higher in cigarette group than in control group (p?<?0.05) and was significantly lower in ALA group than cigarette (p?<?0.05). Protein carbonylation was higher in cigarette group than the control group but not in the non-significant (p?>?0.05). In the ALA it was significantly lower compared to the control group and cigarette (p?<?0.05).

Conclusions: Based on biochemical and histopathological determinations, the study showed that cigarette smoke can cause degenerative effects on skin tissues in rats. However, ALA has a curative effect on cigarette-induced injuries on the skin tissues by anti-oxidative and anti-inflammatory effects.     

Influence of iron on modulation of the antioxidant system in rat brains exposed to lead

The objective of this study was to evaluate markers of oxidative stress in the brains of rats exposed to lead acetate (Pb(C₂H₃O₂)₂), either associated or not associated with ferrous sulfate (FeSO₄). A total of 36 weaning rats (Rattus norvegicus) were divided into 6 groups of six animals and exposed to lead acetate for six weeks. In the control group (control), the animals received deionized water. The Pb260 and Pb260 + Fe received 260 µM lead acetate, and the Pb1050 and Pb1050 + Fe received 1050 µM lead acetate. The Pb260 + Fe and Pb1050 + Fe were supplemented with 20 mg of ferrous sulfate/Kg body weight every 2 days. Group Fe received deionized water and ferrous sulfate. The rat brains were collected to analyze the enzymatic activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and the concentration of reduced glutathione (GSH), lipid peroxidation (TBARS), and total antioxidant substance (TAS) (DPPH^? technique). The activity of SOD and GPx in the experimental groups decreased compared to the control, together with the concentration of GSH (p < 0.05). For CAT analysis, SOD tended to increase in concentration in the experimental groups without a concomitant exposure to FeSO₄, whereas GPx showed a slight tendency to increase in activity compared to the control. For TAS‐DPPH^?, there was a decrease in the experimental groups (p < 0.05). According to the results, SOD, GPx, and GSH were affected by lead acetate and exposure to ferrous sulfate changed this dynamic. However, further studies are needed to verify whether ferrous sulfate acts as a protectant against the toxic effects of lead. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 813–822, 2017.     

Rosmarinic acid exerts a neuroprotective effect in the kainate rat model of temporal lobe epilepsy: Underlying mechanisms

Abstract

Context: Temporal lobe epilepsy (TLE) is an intractable neurological disorder. Rosmarinic acid (RA) is a natural polyphenol with antioxidant, anti-apoptotic, and anti-inflammatory properties.

Objective: This study evaluates beneficial effect of RA in intrahippocampal kainate-induced model of TLE.

Materials and methods: Rats were divided into sham, RA-pretreated sham, kainate, and sodium valproate (VA) or RA-pretreated kainate groups. Rats received RA or VA p.o. at doses of 10 or 300?mg/kg/d, respectively, starting 1?week before the surgery. After 6?weeks, seizure intensity, apoptosis, and oxidative stress markers were evaluated in addition to determination of Timm index as an indicator of mossy fiber sprouting (MFS) and the number of Nissl-stained neurons.

Results: All rats in the kainate group had seizure and 24.3% of rats in the kainate?+?VA group and 36.7% of rats in the kainate?+?RA group showed seizure. The kainate group had a significant elevation of malondialdehyde (MDA) (p?<?0.05) and nitrite (p?<?0.01) and reduction of glutathione (GSH) and catalase activity (p?<?0.05) and pretreatment of kainate-lesioned rats with RA or VA significantly lowered MDA and nitrite content (p?<?0.05) and raised activity of catalase (p?<?0.05). The kainate group also had a significant reduction of neurons in CA1 and CA3 regions and an elevation of Timm index (p?<?0.05–0.001) and RA or VA significantly (p?<?0.05–0.01) prevented these changes.

Discussion and conclusion: RA could attenuate seizure, mitigates oxidative stress, augments the activity of defensive systems, and prevent hippocampal neuronal loss and MFS in the kainate model of TLE.     

Toxic effects of subacute inhalation exposure to trichloroethylene on serum lipid profile,glucose and biochemical parameters in Sprague–Dawley rats

Abstract

The current study evaluated the inhalation toxicity of trichloroethylene (TCE) at 0, 10, 100, 250 and 400?ppm in Sprague–Dawley rats for 10 day period, because the subacute inhalation toxicity of TCE on serum lipid profile, glucose and some biochemical parameters has not been previously reported. TCE vapors were generated using the dynamic generation system based on evaporation method in the exposure chamber. On the basis of the results, mean serum low-density lipoprotein (LDL) and albumin (ALB) decreased significantly in all the groups exposed to TCE compared with the control group (p?<?.005), but there was a significant increase for parameters: fasting blood glucose (FBG) and alkaline phosphatase (ALP) (p?<?.005). Rats exposed to 400?ppm TCE showed a significant decrease in serum cholesterol (CHOL) and protein (Pr) compared with the control group (p?<?.005). A negative relationship was found between triglycerides (TG), very low density lipoprotein (VLDL), CHOL, LDL, Pr, ALB and urea levels and the subacute exposure to concentrations of TCE (R²?=?–0.26, p?<?.05), but there was a direct correlation for parameters FBG, ALP and alanine aminotransferase (ALT) (R²?=?0.42, p?<?.05). In conclusion, studies with Sprague–Dawley rats demonstrated that subacute inhalation exposure to TCE (≥ 100?PPM) is associated with biochemical and lipotoxicity in the form of decreased serum ALB and LDL and raised ALP and glucose levels. The present study also provides additional evidence relating to decreased serum CHOL and Pr after subacute inhalation exposure to 400?ppm TCE.     

Effect of curcumin in mice model of vincristine-induced neuropathy

Abstract

Context: Curcumin exhibits a wide spectrum of biological activities which include neuroprotective, antinociceptive, anti-inflammatory, and antioxidant activity.

Objective: The present study evaluates the effect of curcumin in vincristine-induced neuropathy in a mice model.

Materials and methods: Vincristine sulfate (0.1?mg/kg, i.p. for 10 consecutive days) was administered to mice to induce neuropathy. Pain behavior was assessed at different days, i.e., 0, 7, 10, and 14?d. Sciatic nerve total calcium, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), nitric oxide (NO), and lipid peroxidation (LPO) were also estimated after the 14th day of study. Pregabalin (10?mg/kg, p.o.) and curcumin (15, 30, and 60?mg/kg, p.o.) were administered for 14 consecutive days.

Results: Curcumin at 60?mg/kg significantly attenuated the vincristine-induced neuropathic pain manifestations in terms of thermal hyperalgesia (p?<?0.001) and allodynia (p?<?0.001); mechanical hyperalgesia (p?<?0.001); functional loss (p?<?0.001); and in the delayed phase of formalin test (p?<?0.001). Curcumin at 30 and 60?mg/kg exhibited significant changes (p?<?0.001) in antioxidant levels and in total calcium levels in vincristine-injected mice.

Conclusion: Curcumin at 30 and 60?mg/kg dose levels significantly attenuated vincristine-induced neuropathy which may be due to its multiple actions including antinociceptive, calcium inhibitory, and antioxidant effect.