Oxidative Stress In Wistar Rats Research Articles

Ameliorative effects of Embilica officinalis and Rosmarinus officinalis on cadmium-induced oxidative stress in Wistar rats

The study was designed to assess the antioxidative potential of three dietary antioxidants, vitamin C, Rosemary (Rosmarinus officinalis) leaf extract (10% carnosic acid) and Amla ( Embilica officinalis ) fruit extract (aqueous) on cadmium-induced oxidative stress and the related histopathology of the liver and kidney of Wistar rats. Cadmium was administered as cadmium chloride (15 mg/kg body weight/day) for 4 weeks with five groups co-treated with the antioxidants, vitamin C (100 mg/kg/day) Rosemary leaf extract (15 and 30 mg/kg/day) and amla fruit extract (100 and 200 mg/kg/day). The results showed that cadmium induced a significant increase in both kidney and liver malondialdeyhde (MDA) levels coupled with an inhibition of the superoxide dismutase (SOD) and catalase (CAT) activity. Co-treatment of cadmium and the antioxidants did alleviate the oxidative stress which was observed as a significant reduction in the MDA levels and an increase in the SOD activity both in the kidney and liver. CAT activity was only increased by vitamin C and Rosemary (15 mg/kg) co-treatment in the kidney. Furthermore, cadmium induced cellular disorganization of the kidney and liver was restored with the co-treatment of the antioxidants being more pronounced with the plant extracts. Rosemary leaf extract was efficacious at both the doses while the amla fruit extract had the most ameliorative effect at a higher dose (200 mg/kg).

Subacute chlorpyrifos-induced alterations in serum lipids and some oxidative stress biomarkers in male Wistar rats: beneficial effect of acetyl-L-carnitine

The present study evaluated the beneficial effect of acetyl-L-carnitine (ALC) on subacute chlorpyrifos (CPF)-induced alterations in serum lipid profiles and some biomarkers of oxidative stress in Wistar rats. Twenty-eight adult male rats divided into four groups of seven animals each (group I–IV) were used: I (S/oil) received soya oil (2 ml kg−1), II (ALC) received ALC (300 mg kg−1); III (CPF) received CPF (8.5 mg kg−1 ∼ 1/10th LD50); IV (ALC+CPF) was pretreated with ALC (300 mg kg−1) and then exposed to CPF (8.5 mg kg−1), 30 min later. The treatment was orally for 28 days duration. Sera obtained from blood samples were evaluated for the levels of triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-c), malondialdehyde (MDA), and the activities of superoxide dismutase (SOD) and catalase (CAT). The levels of low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), and atherogenic index (AI) were calculated. The result showed that elevated levels of TG, TC, LDL-c, VLDL-c, AI, and MDA, and the decreased levels of HDL-c, CAT, and SOD induced by CPF were modulated by ALC. It was concluded that ALC ameliorated the alterations in serum lipid and oxidative stress induced by CPF exposure in the rats, partly through its antioxidant properties.

Fish Oil has Beneficial Effects on Behavior Impairment and Oxidative Stress in Rats Subjected to a Hepatic Encephalopathy Model

Hepatic encephalopathy (HE) is a severe neuropsychiatric complication of liver failure, in which there is injury to brain cells, particularly neurons and glia. Brain cells and their function are greatly influenced by omega-3 polyunsaturated fatty acids, essential components of cell membrane phospholipids in the brain that are crucial to normal function. This study assessed the effect of chronic fish oil (FO) supplementation (rich in omega-3 polyunsaturated fatty acids) on behavior and oxidative stress of Wistar rats subjected to HE due to a liver failure caused by thioacetamide (TAA) intoxication. The FO supplementation started in an early phase of brain development, that is, at the 21st day of life, and extended to the 122th day of life. The results indicated that cognitive function, specifically spatial memory, was markedly affected in the group that received TAA. Most notably, the ill effects caused by TAA administration were counteracted by FO supplementation. In addition to behavioral improvements, FO also promoted reduction in levels of thiobarbituric acid-reactive substances and superoxide dismutase activity in hippocampus and cerebral cortex. In summary, FO protected against spatial memory deficits and oxidative stress caused by HE in rats subjected to liver lesion due to TAA intoxication. Further studies are necessary to understand the mechanism underlying FO behaviors in rats subjected to encephalopathy.

Ameliorative Effects of Soya Bean Oil and Vitamin C on Liver Enzymes in Ethanol -Induced Oxidative Stress in Wistar Rats

The protective potential of soya bean oil and vitamin C on Ethanol-induced oxidative stress in Wistar rats was evaluated. Thirty five Wistar rats of both sexes weighing 120-200g were grouped into five groups of seven rats each. Oxidative stress was induced by administration of 20% ethanol (w/v) for 28 days, at the end of the period of administration, the rats were fasted over night and their blood was collected directly from the heart via cardiac puncture in EDTA sample bottles and the blood was centrifuged and the serum was used to determine the levels of of AST, ALT and ALP in all the groups . The result revealed that Ethanol significantly (p<0.05) increased plasma AST, ALT and ALP levels. Vitamin C significantly (p<0.05) decreased serum AST while soya bean oil produced no significant (p<0.05) effect on plasma AST. The serum levels of ALT and ALP were significantly reduced following vitamin C and Soya bean oil administration. The elevation of serum AST, ALT and ALP after alcohol administration is an indication oxidative stress. The decrease in plasma concentration of the liver enzymes after treatment with vitamin C and Soya bean oil reveals the ameliorative potential of vitamin C and soya bean oil against ethanol-induced oxidative stress in Wistar rats.

Effects of Soya Bean Oil and Vitamin C on Lipid Peroxidation and Antioxidant Biomarkers in Ethanol -Induced Oxidative Stress in Wistar Rats.

Effects of Soya Bean Oil and Vitamin C on Lipid Peroxidation and Antioxidant Biomarkers in Ethanol -Induced Oxidative Stress in Wistar Rats.

Methanolic Extract of Musa Sapientum Surker Proffers Antioxidant Effects against Indomethacin-Induced Ulceration Oxidative stress in Wistar Rats

Effect of methanolic extract of musa sapientum sucker (MEMSS) in indomethacin-induced ulceration in Wistar rats was investigated. Thirty albino rats (120-150 g) were divided into six groups. Negative and positive control rats (group 1 and 2) received no treatment and indomethacin (50 mg/kg) respectively. Group 3 rats received Omeprazole (0.8 mg/kg) 4 hours following indomethacin (50 mg/kg) intoxication. Groups 4, 5, and 6 received 5 mg/kg, 10 mg/kg and 20 mg/kg of MEMSS respectively 4 hour after indomethacin (50 mg/kg) induction. Treatment last for fourteen days and dosing was via oral route. Rats were anaesthetized and sacrificed 24 hours following last treatment. In our results, we scored ulcer induction by indomethacin using elevated biomarker enzymes. Indomethacin (50 mg/kg) administered alone increased (p< 0.05) hepatic and renal alanine and aspartate aminotransferases (LALT, LAST and KALT, KAST) by 311.2%, 170.8% and 123.7%, 109.7% respectively when compared with negative control group. Similarly, MEMSS significantly reduced the elevated LALT, LAST and KALT, KAST quantitatively when compared with positive control (IDM) group. MEMSS when administered at graded doses (5, 10 and 20 mg/kg) increased (p< 0.05) catalase levels, liver and kidney SOD levels (p< 0.05) when compared with control groups. 20 mg/kg of MEMSS increased liver and renal reduced glutathione by 69.6% and 32.7% respectively. In conclusion, MEMSS possesses antioxidant benefits against indomethacin-induced ulceration and oxidative stress in rats which could attracts further histomorphological studies.

Protective effect of Trigonella foenum-graecum Linn. on monosodium glutamate-induced dyslipidemia and oxidative stress in rats

Objectives:The present study was designed to evaluate the effect of aqueous extract of Trigonella foenum-graecum(AqE-TFG) seeds on monosodium glutamate (MSG)-induced dyslipidemia and oxidative stress in Wistar rats.Materials and Methods:Neonatal Wistar rats were treated subcutaneously with MSG (4 g/kg b.w.) from day 2 to 14 after birth, on alternate days. After attaining six-weeks of age, MSG-treated rats were administered with AqE-TFG (0.5 and 1 g/kg b.w., orally) or orlistat (10 mg/kg b.w., orally) for 28 days, respectively. Serum chemistry and relevant enzymes in hepato-cardiac tissues were assessed on day 29.Results:AqE-TFG produced significant reduction in serum total cholesterol (TC), triglycerides (TGs), lactate dehydrogenase (LDH), aspartate amino transferase (AST), alanine amino transferase (ALT), hepatic and cardiac lipid peroxides (MDA) levels and elevation in serum high density lipoprotein cholesterol (HDL-C), hepatic and cardiac antioxidant enzymes [glutathione (GSH), and superoxide dismutase (SOD) and catalase (CAT)] levels.Conclusion:Results were comparable with orlistat, a standard anti-obesity drug, and provide clear evidence that the AqE-TFG treatment offered significant protection against MSG-induced dyslipidemia and oxidative stress, and may play an important role in amelioration of the free radical generated consequences like dyslipidemia and atherosclerosis.

Androgen deprivation by flutamide modulates uPAR, MMP-9 expressions, lipid profile, and oxidative stress: amelioration by daidzein

The growth and development of prostate gland is governed by testosterone. Testosterone helps in maintaining the adipose tissue stores of the body. It is well documented that with advancing age there has been a gradual decline in testosterone levels. Our aim was to study the protective role of daidzein on flutamide-induced androgen deprivation on matrix degrading genes, lipid profile and oxidative stress in Wistar rats. Sub-chronic (60 days) flutamide (30 mg/kg b.wt) administration resulted in marked increase in expressions of matrix degrading genes [matrix metalloproteases 9 and urokinase plasminogen activation receptor]. Additionally, it increased the levels of low density lipoproteins, total cholesterol, triglycerides, and lowered the levels of high density lipoproteins and endogenous antioxidant levels. Oral administration of daidzein (20 and 60 mg/kg b.wt) restituted the levels to normal. Daidzein administration resulted in amelioration of the prostate atrophy, degeneracy and invasiveness induced by flutamide. Our findings suggest that the daidzein may be given as dietary supplement to patients who are on androgen deprivation therapy, to minimize the adverse effects related to it and also retarding susceptibility of patients to cardiovascular diseases.

Protective Effect of T. violacea Rhizome Extract Against Hypercholesterolemia-Induced Oxidative Stress in Wistar Rats

The present study examines the effect of methanolic extract of T. violacea rhizomes on high cholesterol (2%) diet fed rats (HCD). At the end of 4 weeks, serum total protein, albumin, reduced glutathione (GSH), and markers of oxidative stress viz., catalase (CAT), superoxide dismutase (SOD), thiobarbituric acid reactive substances (TBARS—a marker of lipid peroxidation), glutathione-S-transferase (GST) and glutathione peroxidase (GPx) in the serum, aorta, liver and heart of HCD and normal rats were assessed and compared. A significant (p < 0.05) elevation in TBARS, and a reduction (p < 0.05) in serum total protein, albumin, GSH and antioxidant enzyme activities was observed in tissues of HCD fed rats compared with the normal group. Co-administration of crude extracts of T. violacea rhizomes protected the liver, heart, serum and aorta against HCD-induced lipid peroxidation in a dose dependant manner. The activities of the extract (500 mg/kg) compared favorably with gemfibrozil. The extracts also protected against HCD-induced reduction in serum total protein, GSH and restored the activities of antioxidant tissues (liver, heart and aorta) enzymes to near normal values. This result suggested that consumption of T. violacea rhizome may help to protect against hypercholesterolemia- induced oxidative stress diseases in the heart and liver.

Selenium and Lycopene Attenuate Cisplatin-induced Testicular Toxicity Associated With Oxidative Stress in Wistar Rats

To investigate the potential protective effects of selenium and lycopene, either alone or in combination, for cisplatin-induced oxidative stress and testicular dysfunction in male rats. A total of 50 adult male Wistar rats were divided into 5 groups of 10 animals each, as follows: control group (treated with placebo); cisplatin-alone group; cisplatin + lycopene group; cisplatin + selenium group; and cisplatin + selenium + lycopene group. The weights and dimensions of testes, epididymes, and accessory glands as well as sperm concentration, motility, and proportion of normal morphology were assessed. Testicular tissue malondialdehyde (MDA) and glutathione (GSH) levels, as well as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities, and plasma testosterone were determined. Cisplatin treatment caused significant reductions in weights and dimensions of testes, epididymes, and accessory glands, sperm concentration, motility, and proportion of normal morphology, enzymatic and nonenzymatic antioxidants, and plasma testosterone levels. There was significantly increased MDA. The co-administration of selenium and lycopene, either separately or in combination, significantly attenuated the harmful effects of cisplatin-induced lipid peroxidation, oxidative stress, loss of genital organ weight and dimensions, as well as function of reproductive organs collectively in the Wistar rat model. The combination of selenium and lycopene was more effective than supplementation of either agent alone in preventing cisplatin-induced testicular damage. Selenium and lycopene supplementation reduced cisplatin-induced testicular toxicity, improved testicular function and prevented cisplatin-related injury to the rat testes by suppression of oxidative stress.

Protective effects of Plantago asiatica L. extract against ferric‐nitrilotriacetate (Fe‐NTA) induced liver oxidative stress in Wistar rats

The Plantago asiatica L.(PA), a native plant in East Asia (Korea, Japan and China etc.), traditionally used as a popular folk for the treatment of liver diseases. The purpose of this study was to evaluate the liver protective effects of PA extract(PAE) on the Ferric‐nitrilotriacetate(Fe‐NTA)‐induced oxidative hepatotoxicity. Fe‐NTA is a potent hepatotoxic agent and has been reported to induce hepatocyte necrosis. The study of liver protection effect that pretreatment with PAE(1, 2, 4 g/kg b.w.) by gavage to Wistar rats for 7 days before a single dose of Fe‐NTA(13.5 mg Fe/kg b.w., i.p.). Only Fe‐NTA treated group showed significantly increased the serum levels of the hepatic enzyme, aspartate aminotransferase(AST) and alanine aminotransferase(ALT) which is representative liver damage marker, and liver tissue malondialdehyde(MDA), product of lipid peroxidation. Moreover, the level of biomarkers indicate the antioxidants status, glutathione(GSH), glutathione‐S‐transferase(GST), glutathione reductase(GR) and superoxide dismutase(SOD) in liver tissue were decreased. However, PAE pre‐treated group showed decreases in the levels of serum AST and ALT and liver tissue MDA in concentration dependent manner and increases in the level of GSH, GST, GR and SOD. These results are significantly different(p&lt;0.05) to compare with only Fe‐NTA treated group. Thus, our study suggested that PAE might contribute to the chemopreventive material against Fe‐NTA‐mediated liver oxidative damage.

Veratric acid ameliorates hyperlipidemia and oxidative stress in Wistar rats fed an atherogenic diet

An investigation was made to reveal the protective effects of veratric acid (VA), a phenolic acid against atherogenic diet-induced hyperlipidemic rats. Male albino Wistar rats were fed with atherogenic diet (4% cholesterol, 1% cholic acid, and 0.5% 2-thiouracil) daily for 30 days and treated with VA (40 mg/kg body weight) daily for a period of 30 days. Rats fed with atherogenic diet showed significant (P < 0.05) elevation in the level of plasma lipids, systolic and diastolic blood pressure, oxidative stress markers (thiobarbituric acid reactive substances, lipid peroxides) and significant (P < 0.05) reduction in the activities of enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic (vitamin C, vitamin E, and reduced glutathione) antioxidants in erythrocytes, plasma, and tissues (liver, kidney, and aorta). Oral administration of VA (40 mg/kg body weight) for 30 days to atherogenic diet fed rats markedly attenuates systolic, diastolic blood pressure and lipid peroxidation products. Further, VA treatment significantly improved enzymatic and non-enzymatic antioxidants levels and showed beneficial effects on lipid profile in atherogenic diet rats. All the above alterations were supported by histopathological observations. These results indicate that oral administration of VA ameliorates atherogenic diet-induced hyperlipidemia in rats by its free radical scavenging; improving the antioxidants and lipid lowering properties.

β-Sitosterol Prevents Lipid Peroxidation and Improves Antioxidant Status and Histoarchitecture in Rats with 1,2-Dimethylhydrazine-Induced Colon Cancer

Oxidative stress has become widely viewed as an underlying condition in diseases such as ischemia/reperfusion disorders, central nervous system disorders, cardiovascular disease, cancer, diabetes, etc. The role that antioxidants play in the process of carcinogenesis has recently gained considerable attention. β-Sitosterol, a naturally occurring sterol molecule, is a relatively mild to moderate antioxidant and exerts beneficial effects in vitro by decreasing the level of reactive oxygen species. The present study evaluated the antioxidant potential of β-sitosterol in 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis. The enzymatic and nonenzymatic antioxidants and lipid peroxides in colonic and hepatic tissues were evaluated. Generation of reactive oxygen species, beyond the body's endogenous antioxidant capacity, causes a severe imbalance of cellular antioxidant defense mechanisms. Elevated levels of liver lipid peroxides by DMH induction were effectively decreased by β-sitosterol supplementation. β-Sitosterol also exhibited a protective action against DMH-induced depletion of antioxidants such as catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione S-transferase, and reduced glutathione in colonic and hepatic tissues of experimental animals. Supplementation with β-sitosterol restored the levels of nonenzymatic antioxidants (vitamin C, vitamin E, and glutathione). Histopathological alterations in DMH-induced animals were restored to near normal in rats treated with β-sitosterol. Thus, β-sitosterol by virtue of its antioxidant potential may be used as an effective agent to reduce DMH-induced oxidative stress in Wistar rats and may be an effective chemopreventive drug for colon carcinogenesis.

Quercetin attenuates lindane induced oxidative stress in wistar rats

A wide number of pesticides, including highly persistent organochlorine compounds, such as lindane (γ-Hexachlorocyclohexane), have deteriorative effect on fauna and flora by inducing oxidative stress. Lindane induces cell damage by producing free radicals and reactive oxygen species. Quercetin, a dietary flavonoid, is ubiquitous in fruits and vegetables and plays an important role in human health by virtue of its antioxidant function. In this study the flavonoid quercetin was used to investigate its antioxidative effect against lindane induced oxidative stress in rats. The level of lipid peroxidation, reduced glutathione (GSH) were analysed in addition to the antioxidant enzymes such as catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione-s-transferase (GST) activities in the liver and kidney tissue. Levels of hepatic marker enzymes in serum like Aspartate transaminase (AST), Alanine transaminase (ALT), Alkaline phosphatase (ALP) and Lactate dehydrogenase (LDH) and renal markers like serum creatinine and serum urea were estimated. Administration of Lindane induced histopathological alterations and increased levels of serum hepatic and renal markers and malondialdehyde (MDA) with a significant decrease in GSH content and CAT, SOD, GPx and GST activities. Cotreatment of quercetin along with lindane significantly decreased the lindane induced alteration in histology, serum hepatic and renal markers and MDA and also improved the cellular antioxidant status. The results show that Quercetin ameliorates Lindane induced oxidative stress in liver and kidney. The quercetin exhibited chemopreventive effect when administered along with lindane.

Efficacy of trans-2-Hydroxycinnamic acid against Trichlorfon-induced oxidative stress in wistar rats

Trichlorfon is an organophosphate insecticide used to control cockroaches, crickets, silverfish, bedbugs, fleas, cattle grubs, flies, ticks, leaf miners, and leaf-hoppers. It is also used to treat domestic animals for control of internal parasites. Trans-2-hydroxycinnamic acid (T2HCA) is a hydroxyl derivative of cinnamic acid. The present study highlights trichlorofon-induced toxicity and the protective role of T2HCA in the liver, kidney, and brain of female Wistar rats. The rats were given a single dose of trichlorofon (150 mg / kg bw) and pre- and post-treatment T2HCA (50 mg / kg bw) for seven days. Trichlorofon enhanced oxidative stress in liver, kidney, and brain of the rats, which was evident from the elevation of lipid peroxidation (LPO). The reduced level of non-enzymatic antioxidant glutathione (GSH) also indicated the presence of an oxidative insult. The activity of enzymatic antioxidants like superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx) was significantly decreased on trichlorfon administration. Pre and post treatment with T2HCA decreased the LPO level and increased SOD, CAT, GST, GR, GPx, and GSH in the brain, liver, and kidney. Trichlorfon-induced reduction in acelylcholinestrase was also ameliorated with T2HCA treatment. In conclusion, trichlorfon-mediated induction in the reactive oxygen species and disturbance in the antioxidant enzymes’ defense system was moderately ameliorated by antioxidant trans-2-hydroxycinnamic acid.

Effect of Chenodeoxycholic Acid on Fibrosis, Inflammation and Oxidative Stress in Kidney in High-Fructose-Fed Wistar Rats

Background: Recent studies indicate farnesoid X receptor (FXR) plays an important role in regulating lipid metabolism in kidney disease. The purpose of the present study is to investigate the effect of chenodeoxycholic acid (CDCA), a FXR agonist, on fibrosis, inflammation and oxidative stress in kidney in rats fed on high fructose. Methods: Twenty-four healthy male Wistar rats were randomly divided into three groups (n=8): normal control group, high fructose group and chenodeoxycholic acid group. Rats were sacrificed by the end of 16 weeks after feeding. Blood urea nitrogen, serum creatinine, fast glucose, lipid concentration were observed, spot urine samples were obtained to measure the albumin and creatinine levels. Triglyceride of renal cortices was detected. The mRNA level and protein contents of the fibrosis-inducing growth factor transforming growth factor β1 (TGF-β1) and plasminogen activator inhibitor (PAI-I), inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), oxidative stress index NADPH oxidase 2 (Nox2) and p22phox in kidney were examined. The pathological changes of kidney were examined by PAS staining and immunohistochemical staining. Electron microscope sections were made to measure glomerular basement membrane (GBM) width. Results: Renal injuries including mesangial expansion, GBM thickness and podocyte foot process effacement were found in fructose-fed Wistar rats, FXR agonist CDCA modulates renal lipid metabolism, decreases proteinuria and improves renal fibrosis, inflammation and oxidation stress. High-fructose-feeding may cause lipid nephrotoxicity through down-regulated farnesoid X receptor and increases expression of profibrotic growth factors, proinflammatory cytokines, and oxidative stress in Wistar rats. Conclusion: FXR activation by chenodeoxycholic acid can prevent the injury in kidney induced by high fructose feeding.

Nootropic activity of acetaminophen against colchicine induced cognitive impairment in rats

Alzheimer’s disease is a devastating neurodegenerative disorder, the most common among the dementing illnesses. Acetaminophen has gaining importance in neurodegenerative diseases by attenuating the dopaminergic neurodegeneration in Caenorhabditis elegans model, decreasing the chemokines and the cytokines and increasing the anti apoptotic protein such as Bcl-2 in neuronal cell culture. The low concentration acetaminophen improved the facilitation to find the hidden platform in Morris Water Maze Test. Also some data suggest that acetaminophen could contribute in neurodegeneration. The present study was aimed to evaluate the effect of acetaminophen against colchicine induced cognitive impairment and oxidative stress in wistar rats. The cognitive learning and memory behaviour was assessed using step through passive avoidance paradigm and acetylcholine esterase activity. The parameters of oxidative stress were assessed by measuring the malondialdehyde, reduced glutathione and catalase levels in the whole brain homogenates. There was a significant memory improvement in the rats received acetaminophen treatment and it has also decreased the acetylcholine esterase enzyme level, confirming its nootropic activity. Acetaminophen neither increases nor decreases the reduced glutathione and catalase in the whole brain homogenates, showing that acetaminophen is devoid of any adverse effect on brain antioxidant defense system.

Long Term Excessive Zn Supplementation Induced Oxidative Stress in Wistar Rats Fed on Semi-Synthetic Diet

The use of Zn as micronutrient in husbandry and agriculture practices and also in baby foods and multivitamin supplements have been increased during the last two decades. However, the effect of long term increasing Zn load on the oxidative stress in the body has not been worked so far. The supplementation of pharmacological dosage of Zn in otherwise Zn adequate diet was investigated with the aim if excess Zn in the diet triggers oxidative stress and its conesquence on enzymes of antioxidant defense system. In this study, three groups of rats were fed on semi-synthetic diet containing 20 mg Zn/kg (control, group-I), 40 mg Zn/kg (group-II) and 80 mg Zn/kg (group-III) diet respectively for a period of 6 months. Blood lipid profile in the serum, lipid peroxidation status and the activities of antioxidant enzymes and trace minerals level were estimated both in the liver and kidney of three groups of rats. The study revealed that the gain in body weight increased in rats in Zn concentration dependent manner. The blood lipid profile displayed a significant rise in serum glucose, total lipids, cholesterol, triglycerides, LDL-cholesterol, VLDL-cholesterol whereas HDL-cholesterol showed a reduction in their levels in group-II and III than their control counter parts. The lipid peroxidation products were higher and the enzyme activities of superoxide dismutase, catalase, glutathione-s-transferase, glutathione reductase, glutathione (reduced) and glucose-6-phosphate dehydrogenase were significantly lowered in liver and kidney of group-II and group-III. Their mineral status revealed a higher Zn concentration and lower Cu, Mg and Mn both in liver and kidney. This data suggest that Zn in excess in diet when fed for longer periods of time induces oxidative stress by altering the status of minerals.

In vivo antioxidant potentials of Stachytarpheta angustifolia leaf extract on acute butylated hydroxytoluene-induced oxidative stress in Wistar rats

In vivo antioxidant potentials of Stachytarpheta angustifolia leaf extract on acute butylated hydroxytoluene-induced oxidative stress in Wistar rats

Lipoic acid and moderate swimming improves the estrous cycle and oxidative stress in Wistar rats

The generation of reactive oxygen species resulting from physical activity may trigger adaptive processes at the reproductive level and in the antioxidant defense system itself. The objective of this study was to investigate the effects of moderate daily swimming and lipoic acid (LA) supplementation on estrous cycle duration and pro-oxident and antioxidant markers in young Wistar rats. Animals were submitted to daily swimming (for 1 h) for 30 days, between 1300 h and 1400 h. The following study groups were formed: group 1, sedentary; group 2, submitted to swimming; group 3, sedentary supplemented with 100 mg·kg(-1)·day(-1) of LA; and group 4, submitted to swimming and supplementation with 100 mg·kg(-1)·day(-1) of LA. The estrous cycle of the animals was evaluated daily, and the following oxidative stress markers were measured: plasma thiobarbituric acid reactive substances (TBARS) and glutathione (GSH), erythrocyte superoxide dismutase (SOD), GSH peroxidase (GPx) and catalase (CAT) activity. The exercise protocol increased estrous cycle duration in group 2, especially in the diestrous phase. There was also a decrease in lipoperoxidation, with enhanced antioxidant activity of SOD and GPx. Group 4 showed no alteration in estrous cycle duration and maintained the beneficial effects on the antioxidant system observed in group 2. The increase in estrous cycle duration and improved oxidative stress markers may be an adaptive response to moderate exercise. LA impeded any exercise-induced alteration in the cycle but preserved improvements in the antioxidant system.