Common onion (Allium cepa) extract reverses cadmium-induced organ toxicity and dyslipidaemia via redox alteration in rats

Background: Cadmium (Cd) remains an important environmental pollutant of public health concern as it causes organ toxicity, and cardiovascular diseases (CVD), but the roles of common foods such as onion (Allium cepa) need further clarification. The aims of this study were to clarify whether or not Cd-induced organ dysfunction was associated with blood protein, lipid and lipid peroxidation and the effects of onion extract AcE in a rat model. Methods: Control and Cd-treated rats were maintained on control diet, while AcE+Cd-treated rats were also orally administered AcE (1 ml/100 g body weight). Cd-treated and AcE+Cd-treated rats also received cadmium as CdSO₄ (1.5 ml/kg body weight of 0.3 mg/L of CdSO₄) via drinking water. Results: It was found that Cd significantly increased total cholesterol, triglycerides, LDL-cholesterol, serum albumin, and reduced HDL-cholesterol, total plasma protein, and plasma testosterone. Administration of AcE restored the liver and kidney toxicities and blood protein and lipid profiles. Moreover, AcE improved Cd-induced decrease in urinary volume and renal clearance, and also protected against Cd-induced oxidative stress by normalizing redox status. However, AcE did not affect Cd-induced altered plasma testosterone. Conclusion: Our study suggests that Cd-induced CVD was associated with altered blood dysproteinemia, dyslipidaemia, and oxidative stress. It also provided the first evidence of the therapeutic efficacy of AcE against atherosclerotic conditions and organ toxicity in Cd-intoxicated rats via a mechanism independent of the circulating testosterone level.     

Reversal of cadmium-induced oxidative stress in rat erythrocytes by selenium,zinc or their combination

The aim of this study was to evaluate the potential benefit of combined treatment with zinc (Zn) and selenium (Se) in reversing cadmium (Cd)-induced oxidative stress in erythrocytes, compared to Se or Zn treatment alone in rats exposed to Cd. For this purpose, 30 adult male Wistar albino rats were equally divided into control and four treated groups received either 200 ppm Cd (as CdCl₂), 200 ppm Cd+500 ppm Zn (as ZnCl₂), 200 ppm Cd+0.1 ppm Se (as Na₂SeO₃), or 200 ppm Cd+500 ppm Zn+0.1 ppm Se in their drinking water for 35 days. Marked alterations of antioxidative system were found in Cd-treated rats. Activities of catalase (CAT) and glutathione peroxidise (GSH-Px) as well as the total glutathione (GSH) contents in erythrocytes were significantly decreased, whereas the activity of total superoxide dismutase (SOD) was significantly increased. The treatment of Cd-exposed rats with Se alone had no significant effect on the Cd-induced increase in the SOD activity but increased significantly the CAT and GSH-Px activities and partially reversed Cd-induced depletion of GSH levels in erythrocytes. The treatment of Cd-exposed animals with Zn alone partially reversed Cd-induced increase in SOD activity and Cd-induced decrease in GSH-Px activity. The combined treatment of Cd-exposed animals with Se and Zn was more effective than that with either of them alone in reversing Cd-induced decrease in CAT and GSH-Px activities and Cd-induced increase in SOD activity. This treatment also partially restored Cd-induced depletion of GSH. These results could be important for the further development of better treatments for people and/or animals exposed to Cd.     

Effect of streptozotocin-induced diabetes on the activity of calcium channels in rat dorsal horn neurons

We have previously found that spinal dorsal horn neurons from streptozotocin-diabetic rats, an animal model for diabetes mellitus, show the prominent changes in the mechanisms responsible for [Ca²⁺]_i regulation. The present study aimed to further characterize the effects of streptozotocin-induced diabetes on neuronal calcium homeostasis. The cytoplasmic Ca²⁺ concentration ([Ca²⁺]_i) was measured in Fura-2AM-loaded dorsal horn neurons from acutely isolated spinal cord slices using fluorescence technique. We studied Ca²⁺ entry through plasmalemmal Ca²⁺ channels during potassium (50 mM KCl)-induced depolarization. The K⁺-induced [Ca²⁺]_i elevation was inhibited to a different extent by nickel ions, nifedipine and ω-conotoxin suggesting the co-expression of different subtypes of plasmalemmal voltage-gated Ca²⁺ channels. The suppression of [Ca²⁺]_i transients by Ni²⁺ (50 μM) was the same in control and diabetic neurons. On the other hand, inhibition of [Ca²⁺]_i transients by nifedipine (50 μM) and ω-conotoxin (1 μM) was much greater in diabetic neurons compared with normal animals.These data suggest that under diabetic conditions the activity of N-and L- but not T-type voltage-gated Ca²⁺ channels substantially increased in dorsal horn neurons.     

Hesperetin protects against oxidative stress related hepatic dysfunction by cadmium in rats

The present study was to evaluate the hepatoprotective effect of hesperetin (HTN) on cadmium (Cd) induced hepatotoxicity in male Wistar rats. Administration of Cd (3 mg/kg body weight/day) subcutaneously for 21 days, the levels of hepatic markers such as aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma glutamyl transferase (GGT) and bilirubin were significantly increased in serum. The levels oxidative stress markers, thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), conjugated dienes (CD) and protein carbonyl content (PCC) were also significantly increased while the levels of vitamin C, vitamin E, reduced glutathione (GSH), total sulphydryl group (TSH) and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD) were significantly decreased in the liver of Cd intoxicated rats. HTN, a flavanone in citrus fruits, administrated orally along with Cd injection for 21 days, significantly revert back the status of serum hepatic markers, oxidative stress markers and antioxidant markers in the liver tissue to near normal level in a dose dependent manner. HTN at a dose of 40 mg/kg body weight/day exhibits significant (p < 0.05) hepatoprotection compared with other two doses (10 and 20 mg/kg body weight/day). The histopathological studies in the liver of rats also supported that HTN (40 mg/kg) markedly reduced the toxicity of Cd and preserved the histoarchitecture of the liver tissue to near normal. Thus, the results suggest that HTN acts as a potent hepatoprotective agent against Cd induced hepatotoxicity in rats.     

Protective effects of nigella sativa against gentamicin-induced nephrotoxicity in rats

The aim of this study was focused on investigating the possible protective effect of NS against GS-induced nephrotoxicity. Twenty four Wistar-albino rats were divided into four equal groups as follows: control group, GS group (100 mg/kg intraperitoneal – i.p.), NSL+GS group (0.2 ml/kg+100 mg/kg i.p.) and NSH+GS group (0.4 ml/kg+100 mg/kg i.p.). Plasma creatinine and urea levels significantly increased as a result of nephrotoxicity in the GS group. Also, creatinine and urea levels significantly decreased in NSL+GS and NSH+GS groups. In the GS group, plasma MDA and NO levels increased significantly (p<0.05) and erythrocyte SOD and GSH-Px activities decreased significantly (p<0.05) when compared with control group. NS administration with GS injection resulted in significantly decreased MDA and NO generation and increased SOD and GSH-Px activities when compared with GS group. Proximal tubular necrosis, vacuolation, desquamation and degeneration in epithelial cells of the proximal tubules, hyaline casts in tubular lumen, mononuclear cell infiltration, glomerular and basement membrane alterations were histopathologically detected in the kidneys of the GS group. Co-treatments with NS (low and high dose) considerably decreased the renal damage when compared with the GS group. In conclusion, NS acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GS both in the biochemical and histopathological parameters.     

Biochemical evaluation of leachate-contaminated groundwater on the kidney of Albino rats

The effect of leachate-contaminated groundwater on the cells of the kidney was evaluated. Serum Na⁺ concentration of control rats was observed to be 120±1.0 nmol/l while that of rat placed on simulated leachate was 180±4.0 nmol/l. Serum K⁺, urea and creatinine concentrations of rats placed on simulated leachate and leachate-contaminated groundwater were significantly higher(p<0.05) than those of control rats. The activity of Alkaline phosphatase (ALP) of the kidney and serum, respectively, observed for the control rats were (237±3.70 and 0.37±0.01)nmol/min/mg protein while (116±4.20 and 3.17±0.20)nmol/min/mg protein was the ALP activity of kidney and serum, respectively, observed for the rats placed on simulated leachate. Histological examination of the kidney of the control rats showed no visible lesion while that of rats placed on simulated leachate showed extensive necrosis of muscle fibres and cellular infiltration by macrophages. It is viewed that leachate-contaminated groundwater may damage kidney cells and impair renal function.     

Does prolonged radiofrequency radiation emitted from Wi-Fi devices induce DNA damage in various tissues of rats?

Wireless internet (Wi-Fi) providers have become essential in our daily lives, as wireless technology is evolving at a dizzying pace. Although there are different frequency generators, one of the most commonly used Wi-Fi devices are 2.4 GHz frequency generators. These devices are heavily used in all areas of life but the effect of radiofrequency (RF) radiation emission on users is generally ignored. Yet, an increasing share of the public expresses concern on this issue. Therefore, this study intends to respond to the growing public concern. The purpose of this study is to reveal whether long term exposure of 2.4 GHz frequency RF radiation will cause DNA damage of different tissues such as brain, kidney, liver, and skin tissue and testicular tissues of rats. The study was conducted on 16 adult male Wistar–Albino rats. The rats in the experimental group (n = 8) were exposed to 2.4 GHz frequency radiation for over a year. The rats in the sham control group (n = 8) were subjected to the same experimental conditions except the Wi-Fi generator was turned off. After the exposure period was complete the possible DNA damage on the rat’s brain, liver, kidney, skin, and testicular tissues was detected through the single cell gel electrophoresis assay (comet) method. The amount of DNA damage was measured as percentage tail DNA value. Based on the DNA damage results determined by the single cell gel electrophoresis (Comet) method, it was found that the% tail DNA values of the brain, kidney, liver, and skin tissues of the rats in the experimental group increased more than those in the control group. The increase of the DNA damage in all tissues was not significant (p > 0.05). However the increase of the DNA damage in rat testes tissue was significant (p < 0.01).In conclusion, long-term exposure to 2.4 GHz RF radiation (Wi-Fi) does not cause DNA damage of the organs investigated in this study except testes. The results of this study indicated that testes are more sensitive organ to RF radiation.     

Protective effect of light emitting diode phototherapy on fluorescent light induced retinal damage in Wistar strain albino rats

BackgroundArtificial light at night alters retinal physiology. Several studies have shown that light emitting diode phototherapy protects the retina from the damaging effects of acute light exposure.ObjectiveThe aim of this study has been to elucidate the protective effects of 670 nm LED light on retinal damage induced by chronic fluorescent light in Wistar rats.MethodsMale Wistar albino rats were divided into four groups: group 1 were control (CL), group 2, 3 and 4 were exposed to fluorescent light (FL), LED preexposure + fluorescent light exposure (LL) and only LED light exposure (OL) respectively. All animals were maintained in their specific exposure regime for 30 days. Fluorescent light of 1800 lx was exposed between 8 pm to 8 am. Rats were exposed to therapeutic LED light of 670 nm of 9 J/cm² at 25 mW/cm² for 6 min duration. Histopathological changes in the retina were studied.ResultsAnimals of the FL group showed a significant reduction in the outer nuclear layer thickness and cell count in addition to the total thickness of the retina. LL group which were exposed to 670 nm LED prior to exposure to fluorescent light showed a significant decrease in the degree of damage.Conclusions670 nm LED light preexposure is protective to retinal cells against fluorescent light-induced damage.     

Protective effects of aqueous extract of Artemisia campestris against puffer fish Lagocephalus lagocephalus extract-induced oxidative damage in rats

The aerial parts of Artemisia campestris are often used in Tunisian poisoning cases and are known to possess significant antioxidant activities. The objective of this study is to evaluate the protective effects of an aqueous extract (5 g/l) of A. campestris leaves and stems (AE), on oxidative damages induced by liver extract (LT) from poisonous fish Lagocephalus lagocephalus in wistar rats. AE was found to contain large amounts of K⁺, Na⁺, Ca⁺⁺ and significant antioxidant capacities highlighted by high level of polyphenols and scavenging activities for DPPH and superoxide anion.LT-injected rats (1 ml/100 g body wt) for 10 days showed (1) a reduced appetite and diarrhea resulting in a lower growth rate than controls, (2) a decrease in serum ALT and AST activities suggesting liver functional disorders, (3) an increase of serum urea and creatinine and reduced serum sodium and potassium concentrations highlighting renal insufficiency and (4) an oxidative stress as evidenced by the raise of TBARS and the inhibition of SOD, CAT and GSH-Px activities in liver, kidney and brain tissuesAbsorption of AE as a drink, for 20 days (10 pre-treatment days+10 experiment days) did not lead significant change of studied parameters but prevented all the disorders induced by LT.     

The effects of orchidectomy on toxicological responses to dietary ochratoxin A in Wistar rats

Ochratoxin A (OTA) causes pathological lesions in the organs of animals. Males are more sensitive to OTA exposure than females but the reasons for this are unknown.The objective of this study was to explore the role of testosterone in male rats with OTA-related pathogenesis. To test the effect of testosterone on OTA toxicity, the testes of a group of rats were surgically removed. Male and female rats (approximately 300 and 200 g) were fed with OTA-contaminated feed (initially approximately 300 μg kg⁻¹ b.w. per day) for 24 weeks. The organs of all the animals were collected and their organ lesion pathology, caspase-3 expression, OTA plasma and organ concentrations and total plasma testosterone concentrations were evaluated. OTA treatment created serious lesions in the kidney, liver and testes of rats. The major histopathological changes in the kidney and liver were karyomegaly, hemorrhages and vacuolization. In the testes, there was a marked decrease in the amount of spermatozoon. The degrees of organ lesion were evaluated and the castrated males had the lowest kidney and liver lesion scores, indicating that testosterone reduction in males dramatically reduces OTA-related organ damage. The plasma OTA levels for the intact males, the castrated and the females were 6.34, 8.42 and 12.5 μg ml⁻¹, respectively.In conclusion, despite the similar plasma OTA levels of the intact and castrated males, OTA is less toxic in the castrated males. Therefore, the well-known gender specific toxicity of OTA seems to be related to the testosterone levels of rats.     

Autumnalamide targeted proteins of the immunophilin family

Previous works with autumnalamide reported that Store Operated Calcium (SOC) channels were blocked through mitochondrial modulation. In the present paper we studied the effect of autumnalamide on ionomycin Ca²⁺ fluxes. Thus, autumnalamide did not modify ionomycin-sensitive intracellular pools while the ionomycin-induced Ca²⁺ influx was blocked with similar potency whether the incubation was done before or after ionomycin-sensitive pools depletion. Nevertheless, autumnalamide was not able to inhibit ionomycin-induced Ca²⁺ influx once the membrane channels were activated. Moreover, the compound efficiently inhibited flufenamic acid (FFA) Ca²⁺ release induced in this organelle but no the next influx. Since in previous work the effect of autumnalamide was inhibited by cyclosporine A (CsA), structures that target this drug were studied. Therefore, the affinity of autumnalamide for cyclophilin D (Cyp D) was examined. The K_D obtained for Cyp D- autumnalamide was 1.51 ± 1.399. Moreover, the K_D for Cyp A- autumnalamide was calculated. The peptide had a similar order of Cyp A binding affinity than CsA (8.08 ± 1.23 and 6.85 ± 1.1 μM respectively). After testing autumnalamide-binding capacity for Cyp A, the activity of this compound on Cyp A pathway was tested. Thus, the effect on interleukin (IL)-2 release on activated T-lymphocytes was checked. Autumnalamide was able to reduce IL-2 levels near to T cells in resting conditions. Next, the effect over calcineurin and NFATc1 was also evaluated. While CsA inhibits both calcineurin and NFATc1, autumnalamide did not produce any effect. From these results we can conclude that, autumnalamide targeted mitochondrion and prevent T-cells from IL-2 production through the modulation of SOC Ca²⁺ channels.     

Quercetin protects against oxidative stress-related renal dysfunction by cadmium in rats

The aim of this study was to investigate the possible protective role of the dietary flavonoid quercetin on cadmium (Cd)-induced nephrotoxicity using biochemical and histopathological approaches. In experimental rats oral administration of CdCl₂ (5 mg/kg) for 4 weeks significantly induced renal damage which was evident from the increased levels of serum urea, uric acid and creatinine with a significant (p<0.05) decrease in creatinine clearance. Cd also significantly (p<0.05) decreased the levels of urea, uric acid and creatinine in urine. Cd-induced oxidative stress in kidney tissue was indicated by the increased levels of renal lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydroperoxides) and protein carbonyl content with a significant (p<0.05) decrease in non-enzymatic (total sulphydryl group, reduced glutathione, vitamin C and vitamin E) and enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR) and glucose 6-phosphate dehydrogenase (G6PD)). Moreover the kidneys of Cd-treated rats showed tubular necrosis, degeneration, dilation, desquamation, thickening of basement membrane and luminal cast formation. Quercetin treatment markedly attenuated the Cd-induced biochemical alterations in serum, urine and renal tissue. Quercetin also ameliorated the Cd-induced pathological changes when compared with Cd-alone-treated group. These data indicate that the natural dietary antioxidant quercetin might have protective effect against Cd-induced nephrotoxicity and oxidative stress in rats.     

The effects of grape seed and colchicine on carbon tetrachloride induced hepatic damage in rats

This study aims to determine the effects of grape seed and colchicine on carbon tetrachloride (CCl₄) induced hepatic damage and on some serum biochemical parameters. Sixty male Wistar albino rats (200–250 g) were randomly divided into six groups (ten rats/group) and included the control group the group were given isotonic sodium chloride (1 mL/kg b.w) intraperitonealy (i.p.), group 2 the group treated i.p. injection of CCl₄ (1.0 mL/kg b.w) in corn oil twice in the first week, Groups 3 and 4 injected with CCl₄ as described for group 2 and the rats were orally given (100 mg/kg b.w) GSE and i.p. injected (10 μg/rat) with colchicine for four weeks, respectively and groups 5 and 6 were the grape seed and colchicine control groups in which rats were orally given grape seed (100 mg/kg b.w) and i.p. injected with colchicine (10 μg/rat), respectively. Anorexia, weight loss, motionlessness and hepatic colour variation at necropsy were observed in groups 2, 3, and 4. Hyperemia, focal bleeding, fat degeneration, changes ranging from degenerative to necrotic, increase in connective tissue elements, pronounced in portal sites in particular, and infiltration of lymphoid series cell observed in the livers of the rats in group 2, treated with CCl₄. Histological hepatic changes in the rats in group 3 and 4 were similar to those in group 2. The levels of serum total protein, albumin and globulin decreased in groups 2, 3, and 4, compared with groups 1, 5 and 6; aspartate transaminase (ALT) activities increased. The lowest alkaline phosphatase (ALP) activities were in groups 4 and 5. We concluded that GSE and colchicine have not sufficient ameliorative effects to CCl₄ induced acute hepatic damage.     

Understanding the influence of MgO and SrO binary doping on the mechanical and biological properties of β-TCP ceramics

The objective of this study was to evaluate the influence of MgO and SrO doping on the mechanical and biological properties of β-tricalcium phosphate (β-TCP). β-TCP was doped with two different binary compositions, 0.25 and 1.0 wt.% SrO along with 1.0 wt.% MgO. MgO and SrO doping increased the β phase stability at a sintering temperature of 1250 °C and marginally decreased the compressive strength of β-TCP. An in vitro cell–material interaction study, using human fetal osteoblast cells (hFOB), indicated that doped β-TCP was non-toxic, and MgO/SrO dopants improved cell attachment and growth. β-TCP implants doped with 1.0 wt.% MgO and 1.0 wt.% SrO showed good in vivo biocompatibility when tested in male Sprague–Dawley rats for 16 weeks. Histomorphology analysis indicated that MgO/SrO-doped β-TCP promoted more osteogenesis than pure β-TCP. In vivo osteocalcin and type I collagen assay also revealed faster bone formation in rats with doped β-TCP implant compared to rats with pure β-TCP implant. Low Ca²⁺ concentration in the urine of rats with doped β-TCP implant confirmed slower degradation of MgO/SrO-doped β-TCP than pure β-TCP.     

Clinico-hematological and micronuclear changes induced by cypermethrin in broiler chicks: Their attenuation with vitamin E and selenium

This study was carried out on 90 one-day-old broiler chicks to know clinico-hematological alterations, DNA damage caused by cypermethrin (CY), and attenuation of toxic effects by vitamin E (Vit E) and selenium (Se). Birds were randomly divided into five equal groups. Groups 1–4 received CY (600 ml kg^?1 b.wt) daily for 30 days by crop tubing. In addition to CY, groups 2, 3 and 4 received Vit E (150 mg kg^?1 b.wt), Se (0.25 mg kg^?1 b.wt), and Vit E (150 mg kg^?1 b.wt)+Se (0.25 mg kg^?1 b.wt), respectively. Group 5 served as control. Birds were monitored twice daily for clinical signs. They were weighed and blood samples were collected at experimental days 10, 20 and 30 for hematological studies. CY-treated birds showed more prominent signs of toxicity compared to CY+Vit E, CY+Se and CY+Vit E+Se birds. Body weight in groups 1–3 was significantly (P<0.05) smaller at days 20 and 30 when compared with the control group. Significantly (P<0.001) higher numbers of micronuclei appeared in chicks treated with CY compared to CY+Vit E- and CY+Se-treated birds. Significantly decreased total erythrocyte counts (TEC), hemoglobin (Hb) concentration and packed cell volume (PCV) in all treated groups were recorded. Treated birds suffered from macrocytic hypochromic anemia. Leukocytosis in early stage and later leucopenia was seen in treated birds. It can be concluded that CY induces toxic effects in broilers chicks; however, these toxic effects can be ameliorated by Vit E or Se. Combination of Vit E and Se was more effective to ameliorate toxic effects of cypermethrin.     

Subcellular localization of glutamate-stimulated intracellular magnesium concentration changes in cultured rat forebrain neurons using confocal microscopy

Glutamate can stimulate increases in intracellular magnesium concentration ([Mg²⁺]_i) and induce neurotoxicity, both independent of Ca²⁺ changes. Although Mg²⁺ is essential within the cell, very little is known about how it is regulated, especially in neurons. Therefore we used the fluorescent indicator, magindo-1 and confocal microscopy to examine possible intracellular pools of Mg²⁺ in cultured neurons that can be dynamically regulated by glutamate. The magindo-1 fluorescence signal was present throughout the cell body and extends into the neuronal processes. The magindo-1 405 nm/490 nm ratio signal was similar in the cytoplasm and nucleus, suggesting that resting [Mg²⁺]_i is uniform across the neuron. The addition of 100 μM glutamate/10 μM glycine in an extracellular Ca²⁺- and Na⁺-free buffer stimulated an increase in [Mg²⁺]_i in both the nuclear and cytoplasmic regions of similar magnitude and duration. This glutamate exposure also stimulated a [Mg²⁺]_i increase in neuronal processes which was inhibited by the N-methyl-d-aspartate receptor antagonist, MK-801 (10 μM). The glutamate-stimulated [Mg²⁺]_i increase in both the cell body and neuronal processes was dependent on the extracellular Mg²⁺ concentration.These findings suggest glutamate-stimulated [Mg²⁺]_i changes may not only impact cytoplasmic processes, but also directly trigger nuclear events involved, for example, in neuronal injury.     

Cadmium-induced hepatotoxicity in rats and the protective effect of naringenin

This experiment pertains to the protective role of naringenin against cadmium (Cd)-induced oxidative stress in the liver of rats. Cadmium is a major environmental pollutant and is known for its wide toxic manifestations. Naringenin is a naturally occurring citrus flavonone which has been reported to have a wide range of pharmacological properties. In the present investigation cadmium (5 mg/kg) was administered orally for 4 weeks to induce hepatotoxicity. Liver damage induced by cadmium was clearly shown by the increased activities of serum hepatic marker enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma glutamyl transferase (GGT) and serum total bilirubin (TB) along with the increased level of lipid peroxidation indices (thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides) and protein carbonyl contents in liver. The toxic effect of cadmium was also indicated by significantly decreased levels of enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (reduced glutathione (GSH), vitamin C and vitamin E). Administration of naringenin at a dose of (50 mg/kg) significantly reversed the activities of serum hepatic marker enzymes to their near-normal levels when compared to Cd-treated rats. In addition, naringenin significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. The histopathological studies in the liver of rats also showed that naringenin (50 mg/kg) markedly reduced the toxicity of cadmium and preserved the normal histological architecture of the tissue. The present study suggested that naringenin may be beneficial in ameliorating the cadmium-induced oxidative damage in the liver of rats.     

An in vivo and in vitro study on the protective effects of N-acetylcysteine on mitochondrial dysfunction in isoproterenol treated myocardial infarcted rats

Altered mitochondrial function plays an important role in the pathology of myocardial infarction. We investigated the protective effects of N-acetylcysteine on mitochondrial dysfunction in isoproterenol induced myocardial infarcted rats. Rats were pretreated with N-acetylcysteine (10 mg/kg) orally daily for 14 days. After pretreatment, rats were induced myocardial infarction by isoproterenol (100 mg/kg) at an interval of 24 h for 2 days. Lipid peroxidation products, antioxidants, lipids, mitochondrial marker enzymes and calcium in the mitochondrial heart were determined. Transmission electron microscopic and in vitro studies were also done. Isoproterenol treatment caused significant increase in mitochondrial lipid peroxides and lipids except phospholipids with significant decrease in mitochondrial antioxidants. Significant decreased activities of marker enzymes and significant increased calcium were observed in mitochondria of myocardial infarcted rats. Pretreatment with N-acetylcysteine showed significant protective effects on all the biochemical parameters and preserved the integrity of heart tissue and restored normal mitochondrial function in myocardial infarcted rats. Transmission electron microscopic findings on the structure of the heart mitochondria confirmed the protective effects and in vitro study also confirmed the antioxidant potential of NAC. The possible mechanism for the improved cardiac mitochondrial function might be due to scavenging free radicals, improving the antioxidant and mitochondrial marker enzymes, maintaining GSH levels, lipids and Ca²⁺ levels by its antioxidant effect. Thus, N-acetylcysteine protected the mitochondrial heart from ISO treated mitochondrial damage. A diet containing N-acetylcysteine may be beneficial to myocardial infarcted heart.     

Effect of short term treatment of L-carnitine on tissue ACE activity in streptozotocin-induced diabetic rats

Diabetes is commonly related to the both microvascular as well as macrovascular complications. It appears that both metabolic and hemodynamic factors interact to create these problems.In this study the effects of orally administered L-carnitine, a natural amino acid, on ACE activity in streptozotocin (STZ)-induced diabetic rats were investigated. Streptozotocin (60 mg/kg body weight) was given intraperitoneally. Fifty male Sprague–Dawley rats were divided into four groups: untreated normal (C), L-carnitine treated normal (CT), untreated diabetics (D), L-carnitine-treated diabetics (DT). CT and DT received daily L-carnitine 1 g/kg orally for 3 weeks after inducing diabetes.The ACE activities in aorta, heart and kidney homogenates was measured at the end of 3 weeks. They were significantly increased in D compared to C group (P < 0.05) and significantly decreased in aorta, heart and kidney in DT compared to D group.In conclusion, L-carnitine can reduce tissue ACE activity in aorta, heart and kidney in streptozotocin diabetic rats, which may be due to higher NO production.     

Protective effect of vitamin E and selenium combination on deltamethrin-induced reproductive toxicity in male rats

The current study was performed to assess the adverse effect of deltamethrin (DLM) on reproductive organs and fertility in male rats and to evaluate the protective role of vitamin E (VE) and selenium (Se) combination in alleviating the detrimental effect of DLM on male fertility. The lethal dose 50 (LD₅₀) of DLM for male rats was estimated at 6 mg/kg bwt. Thirty male albino rats (10-weeks-old) were divided into three groups (10 rats each): Control group was injected subcutaneously with 2 ml/kg bwt saline twice weekly and was daily administered 2 ml distilled water intra-gastrically; DLM-treated group received 0.6 mg/kg bwt (1/10 LD₅₀) DLM intra-gastrically once daily; DLM + VE/Se-treated group was injected subcutaneously with 1.2 mg/kg bwt Viteselen^®15 (VE/Se) twice weekly with concurrent daily administration of 0.6 mg/kg bwt (1/10 LD₅₀) DLM intra-gastrically. The experiment was conducted for 60 consecutive days. DLM caused a significant reduction in reproductive organs weights, sperm count, sperm motility percent, alive sperm percent, serum testosterone level and testicular reduced glutathione concentration (GSH). DLM-treated group showed a significant increase in sperm abnormalities and testicular malondialdehyde (MDA) concentrations. Histopathologically, DLM caused impairments in testes, epididymes and accessory sex glands. Conversely, treatment with VE/Se combination improved the reduction in the reproductive organs weights, sperm characteristics, DLM-induced oxidative damage of testes and the histopathological alterations of reproductive organs. Results indicate that DLM exerts significant harmful effects on male reproductive system and that the concurrent administration of VE/Se partly reduced the detrimental effects of DLM on male fertility.