Hepatoprotection of tea seed oil (Camellia oleifera Abel.) against CCl4-induced oxidative damage in rats.

The oil of tea seed (Camellia oleifera Abel.) is used extensively in China for cooking. This study was designed to evaluate the effects of tea seed oil on CCl(4)-induced acute hepatotoxicity in rats. Male SD rats (200+/-10 g) were pre-treated with tea seed oil (50, 100, and 150 g/kg diet) for six weeks before treatment with a single dose of CCl(4) (50% CCl(4), 2 mL/kg of bw, intraperitoneally), the rats were sacrificed 24h later, and blood samples were collected for assaying serum biochemical parameters. The livers were excised for evaluating peroxidation products and antioxidant substances, as well as the activities of antioxidant enzymes. Pathological histology was also performed. The results showed that a tea seed oil diet significantly (p<0.05) lowered the serum levels of hepatic enzyme markers (alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase), inhibited fatty degeneration, reduced the content of the peroxidation product malondialdehyde, and elevated the content of GSH. Pre-treatment of animals with tea seed oil (150 g/kg diet) could increase the activities of glutathione peroxidase, glutathione reductase and glutathione S transferase in liver when compared with CCl(4)-treated group (p<0.05). Therefore, the results of this study show that a tea seed oil diet can be proposed to protect the liver against CCl(4)-induced oxidative damage in rats, and the hepatoprotective effect might be correlated with its antioxidant and free radical scavenger effects.     

Effects of chronic ingestion of sodium fluoride on myocardium in a second generation of rats

Possible effects of long term exposure (6 months) to sodium fluoride (NaF) through drinking water on the morphology and biochemistry of myocardial tissue in second generation adult male rats were investigated. Wistar strain female and male rats were reared until the second generation of rats obtained, during which they were given 1, 10, 50 and 100 mg/L NaF in drinking water. Of the second generation, 28 male rats were divided into four groups and had the same treatment. All the second generation rats were sacrificed and autopsied at the end of the 6 months. In the samples of myocardial tissues, the levels of serum fluoride and the activities of principal antioxidant enzymes were determined, and a histopathological examination was conducted. Significant histopathological changes were found in the myocardial tissue of rats treated with 50 and 100 mg/L NaF. These were myocardial cell necrosis, extensive cytoplasmic vacuole formation, nucleus dissolution in myosits, swollen and clumped myocardial fibers, fibrillolysis, interstitial oedema, small hemorrhagic areas and hyperaemic vessels. Additionally, the increased activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and thiobarbituric acid-reactive substance (TBARS) levels were observed in the myocardial tissues of rats treated with 10 and 50 mg/L NaF. On the other hand, the activities of SOD, GSH-Px, and CAT decreased, but the TBARS levels increased in the myocardial tissues of rats treated with 100 mg/L. The present results revealed that prolonged ingestion of fluoride through drinking water, particularly with high doses, induced significant histopathological and biochemical changes leading to myocardial tissue damage.     

Effects of chronic administration of S-adenosyl-l-methionine on brain oxidative stress in rats

S-adenosyl-L-methionine (SAM), used to treat liver diseases and as a coadjuvant in antidepressive medication, has neuroprotective effects in animal models. The aim of this study was to discover whether SAM has antioxidant effects in rat brain tissue. Ten male Wistar rats were killed by decapitation and the forebrains incubated with SAM for in vitro experiments. To study the effects of long-term administration, animals in four groups of ten rats each were given 10 mg SAM/kg per day s.c., and 40 other rats were given an equivalent volume of L-lysine (the commercial solvent for SAM). Treatment was started at the end of lactation, and animals were killed by decapitation after 15 days or 1, 6 or 22 months of treatment. The forebrain of each animal was used to test membrane lipid peroxidation by determining thiobarbituric acid-reactive substances (TBARS), glutathione level and enzyme activities related to glutathione (reduced form GSH, oxidized form GSSG) metabolism: GSH-peroxidase (GSHpx), GSSD-reductase (GSSGrd) and GSH-transferase (GSHtf). Chronic treatment with SAM decreased maximum forebrain production of TBARS by 46% compared with animals given L-lysine and increased glutathione levels by 50%, GSHpx activity by 115% and GSHtf activity by 81.4%. The results of in vitro experiments were qualitatively similar: lipid peroxidation was inhibited (13.1+/-1.3 nmol/mg protein in controls vs. 5.9+/-0.8 nmol/mg protein in samples incubated with 1000 micromol/l SAM) and glutathione levels were stimulated (0.97+/-0.06 micromol/g tissue in control samples vs. 1.55+/-0.08 micromol/g tissue in samples incubated with 1000 micromol/l SAM), as were GSHpx and GSHtf. No significant effect was seen in any of the experiments with L-lysine. We conclude that SAM has antioxidant effects in rat brain tissue both in vitro and ex vivo. The effect is seen both as inhibition of lipid peroxide production and as an enhancement of the endogenous glutathione antioxidant system.     

Chronic fluoride toxicity and myocardial damage: antioxidant offered protection in second generation rats

This experiment was designed to investigate the extent of peroxidative changes and histological alterations in the myocardium of rats exposed to high fluoride for two generations, in addition to ameliorative role of selenium and vitamin E on the above indices. Adult albino Wistar rats were given fluoride through drinking water (200 ppm F) and maintained subsequently for two generations, while they were exposed to fluoride throughout the experiment. Fluoride treatment significantly increased the lipid peroxidation and decreased the activity of antioxidant enzymes, viz., catalase, superoxide dismutase, and glutathione level in auricle and ventricle regions of the heart. Decreased feed and water consumption, organ somatic index and marginal drop in body growth rate were observed. Decreased antioxidant enzymes and increased malondialdehyde levels might be related to oxidative damage that occurs variably in the myocardium of rats. Biochemical changes were supported by the histological observations, which also revealed that chronic exposure to fluoride causes damage to the myocardium. Results of this study can be taken as an index of cardio-toxicity in rats exposed to water fluoridation. Further, oral supplementation of selenium and vitamin E not only inhibited oxidative stress but also enhanced the activities of antioxidant enzymes. Administration of antioxidants during fluoride exposure significantly overcame cardiac fluoride toxicity and therefore may be a therapeutic strategy for fluorotic victims.     

Cytoprotective effect of arjunolic acid in response to sodium fluoride mediated oxidative stress and cell death via necrotic pathway

The present study was conducted to investigate the role of arjunolic acid (AA) against sodium fluoride (NaF)-induced cytotoxicity and necrotic cell death in murine hepatocytes. Dose-dependent studies suggest that incubation of hepatocytes with NaF (100mM) for 1h significantly decreased the cell viability as well as intracellular antioxidant power. Besides, NaF administration increased the activities of the membrane leakage enzymes and accumulation of intracellular reactive oxygen species; decreased the activities of the antioxidant enzymes, the glutathione (GSH) and total thiol contents; and elevated the level of oxidised glutathione (GSSG), lipid peroxidation end products as well as protein carbonyl content. In addition to the oxidative impairments, fluoride exposure caused hepatic cell death mainly via the necrotic pathway as supported by the flowcytometric and DNA fragmentation analyses. Incubation with AA (100 microg/ml) both prior to and in combination with NaF almost normalized the altered activities of antioxidant indexes. AA treatment enhanced the cellular antioxidant capability and protected hepatocytes against NaF-induced cytotoxicity and necrotic death. The cytoprotective activity of AA was found to be comparable to that of a known antioxidant, vitamin C. Combining, data suggest that AA plays a protective role against NaF-induced cellular damage and prevents hepatocytes from necrotic death.     

Antidiabetic effect of Punica granatum flowers: Effect on hyperlipidemia,pancreatic cells lipid peroxidation and antioxidant enzymes in experimental diabetes

The present study investigated the effects of Punica granatum aqueous extract (PgAq) on streptozotocin (STZ) induced diabetic rats by measuring fasting blood glucose, lipid profiles (atherogenic index), lipid peroxidation (LPO) and activities of both non-enzymatic and enzymatic antioxidants. Diabetes was induced by single intraperitoneal injection of STZ (60 mg/kg) to albino Wistar rats. The increase in blood glucose level, total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), very low density lipoprotein (VLDL), LPO level with decrease in high density lipoprotein cholesterol (HDL-C), reduced glutathione (GSH) content and antioxidant enzymes namely, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) were the salient features observed in diabetic rats. On the other hand, oral administration of PgAq at doses of 250 mg/kg and 500 mg/kg for 21 days resulted in a significant reduction in fasting blood glucose, TC, TG, LDL-C, VLDL-C and tissue LPO levels coupled with elevation of HDL-C, GSH content and antioxidant enzymes in comparison with diabetic control group.     

Mitigating role of quercetin against sodium fluoride-induced oxidative stress in the rat brain

Context: Quercetin is a well known aglycone flavonoid that is widely found in different food sources.

Objective: In this study, the in vivo neuroprotective potential of quercetin against sodium fluoride-induced oxidative stress was evaluated.

Materials and methods: Wistar rats were divided into five treatment groups and then subjected to daily intraperitoneally treatment with quercetin (at 10 and 20?mg/kg body weight), vitamin C (at 10?mg/kg), or vehicle. After a 1 week treatment period, all groups except saline treated (normal group), were intoxicated with sodium fluoride (NaF) for 1 week. Rat brains were then removed and homogenized for measurement of antioxidant markers including superoxide dismutase (SOD), reduced glutathione, catalase, and lipid peroxidation final products.

Results: The thiobarbituric acid reactive substances (TBARS) levels in the heart homogenate of sodium fluoride treated rats (42.04?±?2.14 nmol MDA eq/g tissue) increased compared to the normal rats (35.99?±?1.08 nmol MDA eq/g tissue). Animals which were pretreated with quercetin at 20?mg/kg for 1 week prior to sodium fluoride intoxication showed significant reduction in the TBARS level (36.13?±?1.12 nmol MDA eq/g tissue). Also, pretreatment with quercetin (20?mg/kg) restored the SOD and catalase activities and modified the level of reduced glutathione compared with the control group (p?>?0.05).

Discussion and conclusion: The present study revealed a potent neuroprotective potential of quercetin against NaF-induced toxicity.     

Antioxidant activity of Albizzia lebbeck (Linn.) Benth. in alloxan diabetic rats

There is an increasing demand for natural anti-diabetic drugs, as continuous oral administration of insulin can culminate in many side effects and toxicity. In our endeavour to formulate some cost-effective herbal medicines for diabetes, we undertook this study to evaluate the antioxidant potential of aqueous extract of Albizzia lebbeck (ALL) in diabetic rats. The oxidative stress in alloxan-induced diabetic rats was determined by estimating the levels of thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and reduced glutathione (GSH) in liver and kidneys. Activities of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione S transferase (GST) were assessed in diabetic as well as rats co-administered with ALL. Oxidative damage in the liver and kidneys of diabetic rats as evidenced by a marked increment in the levels of TBARS and CD, and also a distinct diminution in GSH content was nullified by ALL, as these parameters showed a tendency to retrieve towards normalcy on co-administration of the herbal drug. The antioxidant enzymes registered a decline in activity in diabetic rats thus revealing the damaging effects of free radicals generated due to alloxan exposure. The activities of these enzymes returned to normalcy in ALL-administered rats indicating the antioxidant efficacy of the drug in resisting oxidative insult. The findings provide a rationale for further studies on isolation of active principles and pharmacological evaluation.     

Correlation of testicular toxicity and oxidative stress induced by chlorpyrifos in rats

Effect of chlorpyrifos pesticide on testicular oxidative damage was studied in Sprague-Dawley rats at varying doses. At lower doses (5 and 10 mg/kg body weight/30 days), reduction in plasma levels of testosterone and follicular stimulating hormone (FSH) and luteinizing hormone (LH) along with significant shrinkage of seminiferous tubules and drastic changes in germ cells were seen. But these adverse changes of testes were restored with the revival of serum testosterone and FSH and LH at higher doses (20 and 30 mg/kg body weight/30 days). Similarly, levels of testicular lipid peroxidation and diene conjugates were elevated whereas activities of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase), steroidogenic (Δ(5), 3β-HSD and Δ(5), 17β-HSD) enzymes and angiotensinogen-converting enzyme and glutathione content including lipid-protein content of testes were decreased at low doses. But at higher doses, reductions in level of lipid peroxidation (as revealed by malondialdehyde [MDA] value) and conjugated dienes were found and on the contrary, revivals of testicular antiperoxidative/antioxidant enzymes defense systems, angiotensinogen-converting enzyme (ACE), steroidogenic enzymes, lipid-protein and antioxidant glutathione content were observed. Therefore, the present study indicated from the results that chlorpyrifos had a dual effect at both doses on oxidative stress changes, but at higher doses, the cells were triggering its natural defense mechanism to combat the insult of lower doses of chlorpyrifos and became operative possibly through corrective measure of antioxidant enzymes defense system and pituitary gonadotropins hormones feedback mechanisms on testes.     

Histopathological and biochemical changes in lung tissues of rats following administration of fluoride over several generations

The possible effects of multigenerational administration of sodium fluoride (NaF) via drinking water on lung tissue morphology and biochemistry and body and lung weight were investigated in second-generation adult male rats. For this purpose we selected 45 Albino adult Wistar rats in nine cages, each of which consisted of four females and one male. Twenty-eight pregnant rats were selected for the experiment, divided into four groups of seven rats given 1 (control group), 10, 50 and 100 mg l(-1) NaF in drinking water during the gestation period. After gestation the rats had 165 pups in total. The mothers received fluoridated water during the lactation period and the offspring of the first generation had access to fluoridated water during the suckling period (21 days) and after the weaning period (30 days) until they became mature and at the start of the second part of the experiment. During this time 23 pups died and 79 female and 63 male first-generation rats survived. These first-generation rats were then used to obtain the second-generation offspring in the same manner as before, which were subjected to the same treatments. At the end of 6 months the rats were sacrificed and autopsied. Serum fluoride levels and the activities of principal antioxidant enzymes were determined in lung tissue samples taken from all groups. In addition, the lung tissues were submitted for histopathological examination. Histological findings showed alveolar congestion, alveolar cell hyperplasia and necrosis, prominent alveolar septal vessels, epithelial desquamation and macrophages in the alveolar spaces in the experimental groups. Additionally, there were inflammatory infiltrations in peribronchial, perivascular, intraparenchymal and respiratory tract lumen; intraparenchymal hyperaemic vessels; respiratory epithelial desquamation and proliferation; intraparenchymal thick walled vessels; parenchymal fibrosis; bronchiolitis; pneumonic and focal emphysematous areas. Furthermore, the lung parenchyma was observed to have a distorted appearance with loss of alveolar architecture. These histopathological findings were more pronounced for the rat groups of 50 and 100 mg l(-1) fluoride. No significant histopathological changes were observed in the rats of the control group. The increased activities of superoxide dismutase (SOD) and reduced glutathione peroxidase (GSH-Px) and the decreased activity of catalase (CAT) in the lung tissues with 10 mg l(-1) fluoride might indicate activation of the antioxidant defence mechanism. The decrease in SOD, GSH-Px and CAT activities with 50 and 100 mg l(-1) fluoride and the increase in thiobarbituric acid-reactive substance levels might be related to oxidative damage that occurred in the lung. This multigenerational evaluation of the long-term effect of different doses of fluoride intake through drinking water on lung damage shows that the lung tissues were damaged, there was emphysema and inflammation of lung parenchyma associated with loss of alveolar architecture and the degree of lung damage seemed to correlate with the increased dosage of fluoride. A similar relationship was observed between the degree of lung damage, body and lung weight and serum fluoride levels according to the fluoride dose. Therefore, these results contribute to a better understanding of chronic fluoride toxicity in lung tissue of second-generation rats, especially via drinking water, and the biochemical findings were in agreement with histological observations. In addition, increased fluoride concentration did not affect reproduction or the number of pups dying but the body weight and lung weight ratios were affected by the high dose of fluoride in a dose-related pattern.     

Brain lipid peroxidation and antioxidant status after acute methacrylonitrile intoxication

The status of brain antioxidant enzymes and glutathione in methacrylonitrile (MeAN)-intoxicated Wistar rats was correlated with the levels of lipid peroxidation products. Optimum changes were observed 30 min and 60 min after oral administration of MeAN at dosages of 50 mg/kg body weight per day (0.25 LD50) and 100 mg/kg body weight per day (0.5 LD50). An increase in lipid peroxidation products, decrease in the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione S-transferase (GST), and decrease in reduced glutathione (GSH) were observed. These studies suggest that the membrane lipid peroxidation observed in MeAN intoxication is related, in part, to a compromised antioxidant defense system.     

Aspirin restores normal baroreflex function in hypercholesterolemic rats by its antioxidative action

Besides its well-known effects on platelet aggregation, aspirin has been suggested to be an antioxidant and is also known to improve the lipid profile. In the present study we tested the hypothesis that aspirin by its antioxidant effect, improves haemodynamic profile and baroreflex sensitivity in rat model of hypercholesterolemia. Hypercholesterolemia was induced in Wistar rats by feeding 1% cholesterol rich diet for 10 weeks. Lipid profile, lipid peroxidation and reduced glutathione were estimated in serum. Haemodynamic changes and baroreflex were measured in anaesthetized rats. Hypercholesterolemic rats showed significant increase in total cholesterol, low-density lipoprotein-cholesterol (LDL-C), very low-density lipoprotein-cholesterol (VLDL-C) and atherogenic index and significant decrease in high-density lipoprotein-cholesterol (HDL-C). Significant rise in blood pressure, heart rate and attenuation of baroreflex sensitivity were also found in hypercholesterolemic rat. Aspirin in the dose of 100 mg/kg showed significant decrease in total cholesterol, LDL-C, VLDL-C and atherogenic index and significant increase in HDL-C. Aspirin treatment prevented the rise in blood pressure, heart rate and significantly improved baroreflex sensitivity in hypercholesterolemic rats. Hypercholesterolemic rats showed free radical generation, evident by a significant increase in serum lipid peroxidation and significant reduction in serum reduced glutathione content. Aspirin treatment significantly decreased lipid peroxidation and significantly increased reduced glutathione content. We have demonstrated that aspirin improves baroreflex response and prevents the rise in blood pressure and heart rate possibly by reducing sympathetic activity due to its antioxidant effect in experimentally induced hypercholesterolemic rats.     

Dose dependent protection by lipoic acid against cisplatin-induced ototoxicity in rats: antioxidant defense system.

This study investigated the alterations that occur in auditory brainstem-evoked responses (ABRs) concurrent with changes in cochlear concentrations of glutathione (GSH), lipid peroxidation, and antioxidant enzyme activity in cisplatin-induced ototoxicity and in dose-dependent otoprotection by an antioxidant lipoate. Male Wistar rats were divided into different groups and were treated as follows, with: (1) vehicle (saline) control; (2) cisplatin (16 mg/kg, i.p.); (3) lipoate (100 mg/kg, i.p.) plus saline; (4) cisplatin plus lipoate (25 mg/kg); (5) cisplatin plus lipoate (50 mg/kg), and (6) cisplatin plus lipoate (100 mg/kg). Post-treatment ABRs were evaluated after three days, the rats were sacrificed, and cochleae were harvested and analyzed. The cisplatin-injected rats showed ABR threshold elevations above the pre-treatment thresholds. Rats treated with lipoate plus cisplatin did not show significant elevation of hearing thresholds. Cisplatin administration resulted in a depletion of cochlear GSH concentration (69% of control), whereas, cisplatin-plus-lipoate treatment increased GSH concentration close to control value. Cisplatin-treated rats showed a decrease in cochlear superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) activities (57, 78, 59, and 58% of control, respectively), and an increase in malondialdehyde (MDA) concentration (196% of control). Cochlear SOD, CAT, GSH-Px, and GR activities and MDA concentrations were restored in the rats injected with cisplatin plus graded doses of lipoate than those with cisplatin alone. It is concluded that cisplatin-induced ototoxicity is related to impairment of the cochlear antioxidant defense system, and the dose-dependent otoprotection conferred by an antioxidant lipoate against cisplatin ototoxicity is associated with sparing of the cochlear antioxidant defense system.     

Brain Lipid Peroxidation and Antioxidant Status After Acute Methacrylonitrile Intoxication

The status of brain antioxidant enzymes and glutathione in methacrylonitrile (MeAN)-intoxicated Wistar rats was correlated with the levels of lipid peroxidation products. Optimum changes were observed 30 min and 60 min after oral administration of MeAN at dosages of 50 mg/kg body weight per day (0.25 LD₅₀) and 100 mg/kg body weight per day (0.5 LD₅₀). An increase in lipid peroxidation products, decrease in the activity of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione S-transferase (GST), and decrease in reduced glutathione (GSH) were observed. These studies suggest that the membrane lipid peroxidation observed in MeAN intoxication is related, in part, to a compromised antioxidant defense system.     

Effect of fluoride intoxication on the levels of intestinal antioxidants studied in rats

High concentration of fluorine is noxious to the health of humans and animals. Analysis of fluoride in water samples meant for human consumption in the Vellore District of Tamil Nadu, India, revealed its presence above the permissible limit (4.56 ppm). The present study was aimed to investigate the toxic effects of oral administration of the water sample that contains the highest fluoride content on the status of pathophysiological parameters and lipid peroxidation in experimental rats. A positive control group orally treated with 4.5 ppm of fluoride was also included in the study. The assay of pathophysiological enzymes and histological observations made on the stomach and intestinal tissue have revealed the toxic effects of fluoride intoxication. The observed increase in the levels of thiobarbituric acid reactive substances (TBARS) both in plasma and in intestinal epithelium, with a concomitant decrease in both enzymatic and nonenzymatic antioxidants in the plasma of experimental rats, revealed that the altered antioxidant status during fluoride intoxication may be due to increased free radical generation.     

Prevention of 1,2-dimethylhydrazine-induced circulatory oxidative stress by bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione during colon carcinogenesis

We have performed this study to investigate the modulatory effect of bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione, a bisdemethoxy curcumin analog (BDMCA) on circulatory lipid peroxidation (LPO) and antioxidant status during 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in male Wistar rats. The effects were compared with that of the reference drug, curcumin. Increased tumor incidence as well as enhanced LPO in the circulation of tumor bearing rats was accompanied by a significant decrease in the level of reduced glutathione and activities of glutathione peroxidase (GPx), glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT). Intragastric administration of BDMCA or curcumin to DMH-treated rats significantly decreased colon tumor incidence and the circulatory LPO, with simultaneous enhancement of GSH content and GPx, GST, SOD and CAT activities. We report that BDMCA exert its chemopreventive effect by decreasing the colon tumor incidence as well as by modulating circulatory oxidative stress in DMH-treated rats through its influence on LPO and antioxidant status. The effects of BDMCA were comparable with that of the reference compound curcumin, a well known anticarcinogen and antioxidant. Thus, it would be suggested that the methoxy group is not responsible for the beneficial effects, however, the terminal phenolic moieties or the central 7-carbon chain may play a role.     

Hepatoprotective effect of rhinax on antitubercular drug-induced hepato-toxicity in rats

Rhinax, a polyherbal formulation, exhibited hepatoprotective function when tested against antitubercular drug-induced hepatotoxicity in rats. Suppression of GSH and antioxidant enzymes "superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), gultathionle peroxidase (GPx) and glutathione S-transferase (GST) were noticed in the liver of antitubercular chemotherapeutic agents (namely isoniazid, rifampicin and pyrazinamide) treated animals accompanied with an increase in cytochrome P-450 contents and increased production of lipid peroxidation. Rhinax afforded hepatoprotection by inhibiting lipid peroxidation and, as a result, the animals showed improved antioxidant status.     

Antioxidant role of oils isolated from garlic (Allium sativum Linn) and onion (Allium cepa Linn) on nicotine-induced lipid peroxidation.

Nicotine, a major component of tobacco, is partly responsible for the development of atherosclerosis. It has been suggested that antioxidant nutrients are protective against degenerative diseases. So we have studied the antioxidant effect of oils isolated from onion and garlic on nicotine-induced lipid peroxidation in rat tissues. The lipid peroxidation products and scavenging enzymes were assessed in liver, lungs, heart and kidney. The rats were treated with 0.6 mg nicotine/kg bw and simultaneously given 100 mg garlic or onion oils/kg bw for 21 d. Thiobarbituric acid reactive substances, conjugated dienes and hydroperoxides concentrations were significantly increased in the tissues of nicotine-treated rats. Both the garlic oil and onion oil supplementation to nicotine-treated rats increased resistance to lipid peroxidation. The activities of catalase, superoxide dismutase and glutathione peroxidase decreased in nicotine-treated rats, but there was a trend to increased glutathione content. With garlic oil or onion oil supplementation, nicotine-treated rats had increased activities of antioxidant enzymes and increased concentrations of glutathione. These results indicate that oils of garlic and onion are effective antioxidants against the oxidative damage caused by nicotine.     

Simvastatin attenuates cisplatin-induced kidney and liver damage in rats

Statins have anti-inflammatory effects that are not directly related to their cholesterol-lowering activity. This study aimed to investigate the effect of simvastatin on the extent of tissue damage in cisplatin-induced nephrotoxicity and hepatotoxicity. The rats received a single intravenous injection of 2.5 mg kg⁻¹ cisplatin. Other groups received either simvastatin (1 mg kg⁻¹) or the vehicle (ethanol:saline) intraperitoneally for 10 days beginning 5 days prior to cisplatin injection. All animals were decapitated 5 days after cisplatin administration. Trunk blood was collected and analyzed for blood urea nitrogen (BUN), creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), albumin, and total bilirubin levels. The urine samples were used for the calculation of creatinine clearance levels. The kidney and liver samples were stored for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content or were processed for histopathological examinations. Formation of reactive oxygen species in tissue samples was monitored by using chemiluminescence method. Simvastation reduced the extent of both kidney and liver damage and preserved both kidney and liver functions (p < 0.01–0.001). Increase in liver MDA level with a concomitant reduction in GSH in the cisplatin group was attenuated by simvastatin treatment (p < 0.05–0.01). Increase in tissue collagen content and chemiluminescence levels in the kidney and liver samples of the cisplatin group was also reversed by simvastatin (p < 0.001). In conclusion, simvastatin is beneficial in cisplatin-induced kidney and liver dysfunction and organ damage in rats via prevention of lipid peroxidation and tissue fibrosis, preservation of antioxidant glutathione, and suppression of neutrophil infiltration.     

Protective effects of Phyllanthus amarus aqueous extract against renal oxidative stress in Streptozotocin -induced diabetic rats

Aim and Objectives:

In the present study, we have evaluated the antihyperglycemic, hypolipidemic and antioxidant activities of aqueous extract of Phyllanthus amarus (PAAEt) in streptozotocin (STZ)-induced diabetic rats.

Materials and Methods:

PAAEt was administered at 200 mg/kg body weight/day to normal treated (NT-group) and STZ-induced diabetic treated rats (DT-group) by gavage for eight weeks. During the experimental period, blood was collected from fasted rats at 10 days intervals and plasma glucose level was estimated. The plasma lipid profile was estimated at the end of experimental period. After the treatment, period kidney lipid peroxidation (LPO), protein oxidation and reduced glutathione (GSH) were estimated and antioxidant enzymes viz., glutathione reductase (GR), glutathione peroxidase (GPx) and glutathione-S-transferase (GST), catalase (CAT) and superoxide dismutase (SOD) were also assayed.

Results:

The significant decrease in the body weight, hyperglycemia and hyperlipidemia observed in STZ-induced diabetic rats (D-group) were rectified with PAAEt treatment in diabetic treated group (DT-group). D-group rats showed increased renal oxidative stress with increased LPO and protein oxidation. DT-group showed a significant decrease in renal LPO, protein oxidation and a significant increase in GSH content and GR, GPx and GST activities when compared with D-group. The activities of SOD and CAT decreased significantly in D-group, but were normalized in DT-group. Normal rats treated with PAAEt (NT-rats) showed a significant decrease in lipid profile, renal LPO and protein oxidation, with significant increase in renal GSH and activities of antioxidant enzymes compared to normal rats (N-group).

Conclusion:

Our results demonstrated that PAAEt with its antidiabetic, hypolipidemic and antioxidant properties could be a potential herbal medicine in treating diabetes and renal problems.