Combined effect of ascorbic acid and selenium supplementation on alcohol-induced oxidative stress in guinea pigs

Oxidative stress is a key step in the pathogenesis of ethanol associated liver injury. Ethanol administration induces an increase in lipid peroxidation either by enhancing the production of oxygen reactive species or by decreasing the level of endogenous antioxidants. In this present study, four groups of male guinea pigs (Cavia porcellus) were maintained for 45 days as follows: Control group (1 mg ascorbic acid (AA)/100 g body wt./day); Ethanol group (1 mg AA/100 g body wt./day+900 mg ethanol/100 g body wt./day); Selenium+AA group (25 mg AA+0.05 mg sodium selenite/100 g body wt./day); Ethanol+Se+AA group (25 mg AA+0.05 mg sodium selenite/100 g body wt.+900 mg ethanol/100 g body wt./day). Malondialehyde (MDA), hydroperoxides (HP) and conjugated dienes (CD) were significantly increased, while the activities of scavenging enzymes superoxide dismutase (SOD) and catalase were reduced in the alcohol administered groups. Co-administration of Se+AA along with alcohol increased the activities of scavenging enzymes and reduced the lipid peroxidation products level in hepatic tissues of guinea pigs. Activities of glutathione peroxidase (GPX) and glutathione reductase (GR) were enhanced in co-administered group. gamma-Glutamyl transpeptidase (GGT), a marker enzyme of alcohol induced toxicity, was also reduced, as was the glutathione content. This study suggests that the combined effect of Se+AA, provides protection against alcohol-induced oxidative stress as evidenced from the decreased levels of lipid peroxidation products and enhanced activities of scavenging enzymes.     

Hepatoprotective effect of aqueous extract of Phyllanthus niruri on nimesulide-induced oxidative stress in vivo

Nimesulide (NIM), an atypical non-steroidal anti-inflammatory drug (NSAID) is also used as analgesic. In the present study, we evaluated its effect on the prooxidant-antioxidant system of liver and the hepatoprotective potential of aqueous extract of the herb Phyllanthus niruri (PN) on NIM-induced oxidative stress in vivo using a murine model, by determining the activities of hepatic anti-oxidant enzymes superoxide dismutase (SOD) and catalase (CAT), levels of reduced glutathione (GSH) and lipid peroxidation (expressed as malonaldialdehyde, MDA). Aqueous extract of PN at a dose of 50 or 100 mg/kg body wt was administered either intraperitoneally or orally for 7 days, before NIM administration at a dose of 8 mg/kg body wt twice daily for 7 days in mice. Animals were sacrificed 24 h after administration of final dose of NIM. In another set of experiments, both aqueous extract of PN (at a dose of 50 or 100 mg/kg body wt) and NIM (8 mg/kg body wt) were administered simultaneously for 7 days. Animals were sacrificed 24 h after administration of final dose of the extract and NIM, liver tissues were collected, and the activities of SOD and CAT and levels of GSH and lipid peroxidation end-product (as MDA), were determined from the livers of all the experimental animals. Appropriate NIM control was maintained for all sets of experiments. NIM administration (8 mg/kg body wt) for 7 days caused significant depletion of the levels of SOD, CAT and reduced GSH, along with the increased levels of lipid peroxidation. Intraperitoneal administration of the extract at a dose of 50 mg/kg body wt for 7 days,. prior to NIM treatment, significantly restored most of the NIM-induced changes and the effect was comparable to that obtained by administering 100 mg/kg body wt of the extract orally. Thus, results suggested that intraperitoneal administration of the extract could protect liver from NIM-induced hepatic damage more effectively than oral administration. Antioxidant property of the aqueous extract of PN was also compared with that of a known potent antioxidant, vitamin E. The PN extract at a dose of 100 mg/kg body wt along with NIM was more effective in suppressing the oxidative damage than the PN extract at a dose of 50 mg/kg body wt. Results suggested that beneficial effect of the aqueous extract of PN, probably through its antioxidant property, might control the NIM-induced oxidative stress in the liver.     

Effects of aluminum sulphate and citric acid ingestion on lipid peroxidation and on activities of superoxide dismutase and catalase in cerebral hemisphere and liver of developing young chicks

Effect of oral administration of aluminum sulphate (200 and 400 mg/kg body wt/day) without or with citric acid (62 mg/kg body wt/day) to day-old White Leghorn male chicks (n = 5 per group) for 30 days was studied on the activities of superoxide dismutase (SOD) and catalase, and level of lipid peroxidation in cerebral hemisphere and liver. A 400 mg dose of Al in the presence of citric acid inhibited cytosolic total and CN^--sensitive superoxide dismutase activities of the cerebral hemisphere in 7- and 30-day treated chicks, whereas in 15-day treated chicks the enzyme activities were decreased in response to both doses in the presence of citric acid. In case of liver, activities of these enzymes significantly decreased after 7, 15 and 30 days of treatment with 200 and 400 mg Al together with citric acid, whereas 400 mg Al alone inhibited the enzyme activities after 15 and 30 days of treatment. Cerebral catalase activity decreased in response to 400 mg Al when the chicks were also fed with citric acid for 7 and 30 days, but in 15-day treated chicks the enzyme activity was depleted following treatment with 200 and 400 mg Al combined with citric acid. 400 mg Al treatment for 7 days in combination with citric acid inhibited hepatic catalase activity and extension of the treatment period to 15 and 30 days also produced reduction in its activity even in response to the lower Al dose mixed with citric acid. CN^--insensitive SOD activity of cerebral hemisphere and liver was unaffected by Al. Al also failed to induce lipid peroxidation in both the tissues throughout the course of exposure. Activities of SOD and catalase of cerebral hemisphere and liver of 30-day old chicks were observed to be inhibited by in vitro incubation with different concentrations of Al. Our in vivo study demonstrates that only CN^--sensitive SOD is susceptible to Al. Further, responses of SOD and catalase to Al is tissue specific. The observed inhibition of antioxidant enzyme activities by A1 is suggestive of a prooxidant state. Induction of such an oxidative condition of the tissues may be attributed to a direct effect of the metal on enzyme molecules or in their synthesis.     

Impact of chromium on lipoperoxidative processes and subsequent operation of the glutathione cycle in rat renal system.

Oral administration of K2Cr2O7 to male albino rats at an acute dose of 1500 mg/kg body wt/day for 3 days brought about sharp decrease in the activities of glucose-6-phosphate dehydrogenase and glutathione reductase of kidney epithelial cells. The scavenging system of kidney epithelium is also affected as evident by the highly significant fall in the activities of glutathione peroxidase, superoxide dismutase and catalase which ultimately leads to the increase in lipid peroxidation value in kidney cortical homogenate. However, glutathione-s-transferase activity in cytosol and glutathione and total thiol content in cortical homogenate were not altered. Chronic oral administration of K2Cr2O7 (300 mg/kg body wt/day) for 30 days to rats lead to elevation in the activities of glutathione peroxidase, glutathione reductase, glutathione-s-transferase, superoxide dismutase and catalase with no change in glucose-6-phosphate dehydrogenase activity in epithelial cells. This might lead to the increase in glutathione and total thiol status and decrease in lipid peroxidation value in whole homogenate system.     

Antihyperglycemic activity of Tarralin™, an ethanolic extract of Artemisia dracunculus L.

The studies reported here were undertaken to examine the antihyperglycemic activity of an ethanolic extract of Artemisia dracunculus L., called Tarralin in diabetic and non-diabetic animals. In genetically diabetic KK-A(gamma) mice, Tarralin treatment by gavage (500 mg/kg body wt./day for 7 days) lowered elevated blood glucose levels by 24% from 479+/-25 to 352+/-16 mg/dl relative to control animals. In comparison, treatment with the known antidiabetic drugs, troglitazone (30 mg/kg body wt./day) and metformin (300 mg/kg body wt./day), decreased blood glucose concentrations by 28% and 41%, respectively. Blood insulin concentrations were reduced in the KK-A(gamma) mice by 33% with Tarralin, 48% with troglitazone and 52% with metformin. In (STZ)-induced diabetic mice, Tarralin treatment, (500 mg/kg body wt./day for 7 days), also significantly lowered blood glucose concentrations, by 20%, from 429+/-41 to 376+/-58 mg/dl relative to control. As a possible mechanism, Tarralin was shown to significantly decrease phosphoenolpyruvate carboxykinase (PEPCK) mRNA expression by 28% in STZ-induced diabetic rats. In non-diabetic animals, treatment with Tarralin did not significantly alter PEPCK expression, blood glucose or insulin concentrations. The extract was also shown to increase the binding of glucagon-like peptide (GLP-1) to its receptor in vitro. These results indicate that Tarralin has antihyperglycemic activity and a potential role in the management of diabetic states.     

Effects of Exogenous Selenium on Nicotine-Induced Oxidative Stress in Rats

The effect of two different doses of selenium [1 and 50 μg selenium/100 g body weight (wt)] on nicotine-induced oxidative damage in liver was investigated in experimental rats. Male albino rats were maintained for 60 days as follows: (1) control group (normal diet), (2) nicotine group (0.6 mg/kg body wt)/day, (3) high-dose selenium (50 μg/100 g body wt)/day, (4) high-dose selenium (50 μg/100 g body wt) + nicotine (0.6 mg/kg body wt)/day, (5) low-dose selenium (1 μg/100 g body wt)/day, and (6) low-dose selenium (1 μg/100 g body wt) + nicotine (0.6 mg/kg body wt)/day. Nicotine administration caused a decrease in the activity of antioxidant enzymes, an increase in the concentration of lipid peroxidation products and protein carbonyls and an increase in the activity of nitric oxide synthase compared to the control group. Coadministration of nicotine and selenium reduced the concentration of lipid peroxidation products and increased the activity of antioxidant enzymes compared to the nicotine group. Selenium also enhanced the metabolism of nicotine. The antioxidant effect was more significant in the group administered a low dose of selenium.     

Taurine protects against carbon tetrachloride toxicity in the cultured neurons and in vivo

Carbon tetrachloride (CCl4) has been found to induce cellular damage by generating oxygen free radicals. A study was carried out to investigate the effects of taurine (extracted from Pegasus laternarius Cuvier) on CCl4 intoxicated cultured neurons. CCl4 application (0.4 mmol x l(-1), 0.8 mmol x l( -1), 1.2 mmol x l (-1) and 1.6 mmol x l(-1 )) increased the lipid peroxidation product and decreased glutathione peroxidase (GPx) activity significantly in a concentration dependent manner. Pretreatment of cultures with taurine (10 micromol x l(-1), 30 micromol x l(-1) and 60 micromol x l(-1)) prevented the loss of GPx activity and lipid peroxidation. The effects of three different dosages of taurine (10 mg/kg body wt., 20 mg/kg body wt. and 40 mg/ kg body wt.) for 45 days on the activities of superoxide dismutase and glutathione peroxidase were examined in the cerebrum, cerebellum and medulla of normal and CCl4 treated mice. Treatment of mice with taurine provided protection against CCl4 toxicity as was evident by lipid peroxide status. Taurine was not so successful at inducing the activity of SOD in normal animals except in the medulla where it could increase the activity of SOD (p < 0.05). Taurine induces the GPx activity in a dose dependent manner in all regions of the brain studied. Also in the CCl4 poisoned mice taurine could augment the status of GPx activity in a dose dependent manner. Hence it is concluded that taurine can protects neurons from the oxidative stress induced by CCl4.     

Hypoglycemic effect of methanol extract of Phyllanthus amarus Schum & Thonn on alloxan induced diabetes mellitus in rats and its relation with antioxidant potential

Methanolic extract of P. amarus was found to have potential anti-oxidant activity as it could inhibit lipid peroxidation, and scavenge hydroxyl and superoxide radicals in vitro. The amount required for 50% inhibition of lipid peroxide formation was 104 microg/ml and the concentrations needed to scavenge hydroxyl and superoxide radicals were 117 and 19 microg/ml respectively. The extract was found to reduce the blood sugar in alloxan diabetic rats at 4th hr by 6% at a dose level of 200 mg/kg body wt and 18.7% at a concentration of 1000 mg/kg body wt. Continued administration of the extract for 15 days produced significant (P < 0.001) reduction in blood sugar. On 18th day after alloxan administration values were almost similar to normal in the group taking 1000 mg/kg body wt.     

Toxicity of endosulfan on kidney of male rats in relation to drug metabolizing enzymes and microsomal lipid peroxidation

Endosulfan administration (po, 15 and 30 days at 7.5 and 10 mg/kg body wt respectively) inhibited the activity of microsomal mixed function oxidases in kidney tissue of male rats. Microsomal and cytosolic protein contents of kidney were significantly increased following 30 days endosulfan exposures. Profound induction in the activity profiles of alcohol dehydrogenase and cytosolic glutathione s-transferase was noticed, however, no such change was apparent in the activity of aldehyde dehydrogenase. Microsomal preparations from treated animals showed a dose and duration dependent increase in spontaneous lipid peroxidation. The observed biochemical changes persisted even after 7 days normalcy allowance provided after the endosulfan (10 mg/kg body wt) withdrawl. The results suggest a substantial renal toxicity of endosulfan to male rats in relation to microsomal mixed function oxidases and associated functions which possibly resulted from lipid peroxidative damage of microsomal membrane in treated animals.     

Biochemical effects of garlic protein on lipid metabolism in alcohol fed rats

Garlic protein is a very good hypolipidemic agent. In the present study the water soluble protein fraction of garlic was investigated for its effect on hyperlipidemia induced by alcohol (3.76 g/kg. body wt./day). The hypolipidemic action is mainly due to an increase in cholesterol degradation to bile acids and neutral sterols and mobilization of triacyl glycerols in treated rats. Garlic protein (500 mg./kg body wt./day) showed significant hypolipidemic action comparable with a standard dose of gugu-lipid (50 mg./kg. body wt./day).     

The modulatory influence of p-methoxycinnamic acid, an active rice bran phenolic acid, against 1,2-dimethylhydrazine-induced lipid peroxidation, antioxidant status and aberrant crypt foci in rat colon carcinogenesis

We investigated the chemopreventive effect of p-methoxycinnamic acid (p-MCA), an active phenolic acid of rice bran, turmeric, and Kaemperfia galanga against 1,2-dimethylhydrazine-induced rat colon carcinogenesis. Male albino Wistar rats were randomly divided into six groups. Group 1 consisted of control rats that received a modified pellet diet and 0.1% carboxymethyl cellulose. The rats in Group 2 received a modified pellet diet supplemented with p-MCA [80 mg/kg body weight (b.wt.) post-orally (p.o.)] everyday. The rats in Groups 3-6 received 1,2-dimethylhydrazine (DMH) (20 mg/kg b.wt.) via subcutaneous injections once a week for the first 4 weeks; additionally, the rats in Groups 4, 5 and 6 received p-MCA at doses of 20, 40 and 80 mg/kg b.wt./day p.o., respectively, everyday for 16 weeks. The rats were sacrificed at the end of the experimental period of 16 weeks. The DMH-treated rats exhibited an increased incidence of aberrant crypt foci (ACF) development; an increased crypt multiplicity; decreased concentrations of tissue lipid peroxidation markers such as thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and lipid hydroperoxides (LOOH); decreased levels of tissue enzymic antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR); and decreased levels of non-enzymic antioxidants such as reduced glutathione (GSH) and vitamins C, E and A in the colon. Supplementation with p-MCA significantly reversed these changes and significantly inhibited the formation of ACF and its multiplicity. Thus, our findings demonstrate that p-MCA exerts a strong chemopreventive activity against 1,2-dimethylhydrazine-induced colon carcinogenesis by virtue of its ability to prevent the alterations in DMH-induced circulatory and tissue oxidative stress and preneoplastic changes. p-MCA was more effective when administered at a dose of 40 mg/kg b.wt. than at the other two doses tested.     

Cardioprotective effect of alpha-mangostin, a xanthone derivative from mangosteen on tissue defense system against isoproterenol-induced myocardial infarction in rats

Increased oxidative stress and antioxidant deficit have been suggested to play a major role in isoproterenol-induced myocardial infarction. The present study was designed to evaluate the effect of alpha-mangostin on the antioxidant defense system and lipid peroxidation against isoproterenol-induced myocardial infarction in rats. Induction of rats with ISO (150 mg/kg body weight, ip) for 2 days resulted in a marked elevation in lipid peroxidation, serum marker enzymes (LDH, CPK, GOT, and GPT) and a significant decrease in the activities of endogenous antioxidants (SOD, CAT, GPx, GST, and GSH). Pre-treatment with alpha-mangostin (200 mg/kg of body weight per day) orally for 6 days prior to the ISO administration and 2 days along with ISO administration significantly attenuated these changes when compared to the individual treatment groups. These findings indicate the protective effect of alpha-mangostin on lipid peroxidation and antioxidant tissue defense system during ISO-induced myocardial infarction in rats.     

N-acetylcysteine exposure on lead-induced lipid peroxidative damage and oxidative defense system in brain regions of rats

Lead (Pb) is known to disrupt the pro-oxidant/antioxidant balance of tissues, which leads to biochemical and physiological dysfunction. Oxidative stress is considered a possible molecular mechanism involved in Pb neurotoxicity. Considering the vulnerability of the brain to oxidative stress under Pb neurotoxicity, this study investigated the effects of exposure of the thiol antioxidant N-acetylcysteine (NAC) on lead-induced oxidative damage and lipid peroxidation in brain regions of the rat. Wister strain rats were exposed to lead in the form of lead acetate (20 mg/kg body wt/d) for a period of 2 wk and the effects of NAC on lead-induced neurotoxicity in rat brain regions were assessed by postadministration of NAC (160 mg/kg body wt/d) for a period of 3 wk. The lipid peroxidation byproduct, malondialdehyde (MDA) increased following lead exposure in both of the regions, and the antioxidant capacities of the cell in terms of the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) was diminished. Following NAC treatment, lead-induced lipid peroxidation decreased and antioxidant enzyme activities improved, with CAT showing enhancement in the cerebral region only and SOD showing enhancements in the cerebellar region. Our result suggests that thiol-antioxidant supplementation following Pb exposure might enhance the reductive status of brain regions by arresting the lipid peroxidative damage in brain regions.     

Synergistic interactions of Ferulic acid with Ascorbic acid: Its cardioprotective role during isoproterenol induced myocardial infarction in rats

Studies on the lipid peroxidation and antioxidant changes and their significance during myocardial injury have provided a new insight into the pathogenesis of heart disease. The heart failure subsequent to myocardial infarction may be associated with an antioxidant deficit as well as increased myocardial oxidative stress. The present study was designed to evaluate the effect of the combination of ferulic acid and ascorbic acid on antioxidant defense system and lipid peroxidation against isoproterenol (ISO)-induced myocardial infarction in rats. Induction of rats with isoproterenol (150 mg/kg body weight daily, i.p.) for 2 days resulted in a marked elevation in lipid peroxidation, serum marker enzymes (LDH, CPK, GOT, and GPT), and a significant decrease in activities of endogenous antioxidants (SOD, GPx, GST, CAT, and GSH). Pre-co-treatment with the combination of ferulic acid (20 mg/kg body weight/day) and ascorbic acid (80 mg/kg body weight/day) orally for 6 days, significantly attenuated these changes when compared to the individual treatment groups. Histopathological observations were also in correlation with the biochemical parameters. Thus, ferulic acid and ascorbic acid significantly counteracted the pronounced oxidative stress effect of ISO by the inhibition of lipid peroxidation, restoration of antioxidant status, and myocardial marker enzymes levels. In conclusion, these findings indicate the synergistic protective effect of ferulic acid and ascorbic acid on lipid peroxidation and antioxidant defense system during ISO-induced myocardial infarction and associated oxidative stress in rats.     

Effect of alpha-tocopherol on doxorubicin-induced changes in rat liver and heart microsomes.

Rats were treated with doxorubicin (2.5 mg/kg body wt, iv) once a week for 8 weeks. Alpha-Tocopherol (400 mg/kg body wt/day) was co-administered orally for 2 months. Cytochrome-P450 (Cyt-P450) and Cytochrome-b5 (Cyt-b5) levels decreased significantly in doxorubicin treated rats. Significant decreases were observed in glucose-6-phosphatase, Cyt-P450 and Cyt-b5 reductase activities. In vitro lipid peroxidation study showed that alpha-tocopherol significantly minimises the lipid peroxide formation by doxorubicin. There was a significant change in microsomal cholesterol and phospholipid levels. Alpha-Tocopherol co-administration reduced the alterations in xenobiotic metabolising system and microsomal lipid levels. The results were discussed with reference to drug metabolising enzymes, lipid peroxidation and antioxidant nature of alpha-tocopherol.     

Aluminium related changes in brain histology: protection by calcium and nifedipine

Aluminium (Al; 50 mg AlCl3/kg body wt/day) treatment caused a marked change in histological picture of normal brain as indicated by an increased number of vacuolated spaces. These changes returned to normal partially by simultaneous treatment with nifedipine (0.7 mg/kg body wt/day) and completely by similar treatment with 50 ppm calcium (CaCl2; 12.5 mg/kg body wt./day). Neither nifedipine nor calcium treatment alone altered the normal histological condition. The histological changes could not be correlated with the decrease in calcineurin activities in brain as nifedipine decreases calcineurin activity without any histological changes. Hence the histological changes may be considered as specific for Al and not due to a general decrease in calcineurin activity.     

Methamphetamine and lipid peroxidation in the rat retina

BACKGROUND: The use of psychoactive drugs during adolescence and early adult life has increased in the last few decades. It is known that developmental exposure to psychostimulants affects the sensory systems, and the retina has been shown to be a target tissue. This work was conducted to evaluate the pattern of lipid peroxidation in the rat retina following prenatal exposure to methamphetamine (MA). METHODS: Pregnant female Wistar rats were given MA (5 mg/kg of body weight/day; SC, in 0.9% saline) from GD 8 to 22. Offspring were sacrificed at postnatal days (PNDs) 7, 14, and 21. The retinas were homogenized, and both the total antioxidant and superoxide dismutase (SOD) activities were measured by enzymatic-colorimetric methods. The lipid peroxidation byproducts (malondialdehyde [MDA] and MDA-like metabolites) were measured by the thiobarbituric acid test. RESULTS: Total antioxidant levels were lower in the MA group at PND 21 in both males and females. The activity of SOD was higher in PND 7 females from the MA group. MDA levels were higher in the MA group at PND 21 in both genders. CONCLUSIONS: These findings suggest that prenatal-induced MA toxicity in the retina may be related to lipid peroxidation processes and oxidative stress.     

Protective effects of thymol on altered plasma lipid peroxidation and nonenzymic antioxidants in isoproterenol-induced myocardial infarcted rats

This study evaluates the protective effects of thymol on altered plasma lipid peroxidation products and nonenzymic antioxidants in isoproterenol (ISO)‐induced myocardial infarcted rats. Male albino Wistar rats were pre and cotreated with thymol (7.5 mg/kg body weight) daily for 7 days. ISO (100 mg/kg body weight) was subcutaneously injected into rats on 6th and 7th day to induce myocardial infarction (MI). Increased activity/levels of serum creatine kinase‐MB (CK‐MB), plasma thiobarbituric acid reactive substances, lipid hydroperoxides, and conjugated dienes with decreased levels of plasma reduced glutathione (GSH), vitamin C, and vitamin E were observed in ISO‐induced myocardial infarcted rats. Pre and cotreatment with thymol (7.5 mg/kg body weight) showed normalized activity of serum CK‐MB and near normalized levels of plasma lipid peroxidation products, reduced GSH, vitamin C, and vitamin E in myocardial infarcted rats. Furthermore, the in vitro study on reducing power of thymol confirmed its potent antioxidant action. Thus, thymol protects ISO‐induced MI in rats by its antilipid peroxidation and antioxidant properties. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:368–373, 2012; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21431     

含微囊藻毒素的蓝藻水华提取物对小鼠抗氧化酶的毒性作用

在世界范围内发生的富含营养的废水中生长蓝藻水华已经造成了严重的水污染。已有报道显示水华中的有毒成分是一类单环七肽微囊藻毒素,它们对人和家畜有严重的毒害作用,本文所使用的蓝藻水华采集于我国的太湖地区。我们采用三个亚致死计量(16、32、64 mg冻干藻细胞/kg体重,相当于4.97、9.94、19.88μg藻毒素/kg体重)的蓝藻水华提取物(CBE),分析它们对小鼠肝脏抗氧化酶的影响。经过连续14d每天腹腔注射CBE,小鼠分别在第3、5、7、9、11、13、15天处死并检测三种主要的抗氧化酶:超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽巯基转移酶(GST)的活性。SOD和CAT的活性均呈现了抑制效应,GST的活性也发生了明显的变化。为了进一步确定过氧化的程度,我们又通过检测丙二醛的含量分析了脂质过氧化的程度。经过14d CBE处理后脂质过氧化表现出了明显的浓度依赖性的上升趋势。我们的结果表明,CBE对小鼠的抗氧化酶有严重毒害作用,并且能够引起脂质的过氧化。     

Oleic Acid Alleviates Cadmium-Induced Oxidative Damage in Rat by Its Radicals Scavenging Activity

Toxic heavy metal cadmium wildly pollutes the environment and threats the human health. Effective treatment of cadmium-induced toxicity and organ damage is an important issue. Cadmium causes organ damage through inducing oxidative stress. Our previous study also found oleic acid (OA) synthesis-related gene can confer resistance to cadmium and alleviate cadmium-induced stress in yeast. However, its alleviation mechanism on cadmium stress especially in animals is still unclear. In this study, the alleviative effects of OA on cadmium and cadmium-induced oxidative stress in rats were investigated. Oral administration of 10, 20, and 30 mg/kg/day OA can significantly increase the survival rate of rats intraperitoneally injected with 30 mg/kg/day cadmium continuously for 7 days. Similar to ascorbic acid (AA), OA can significantly reduce the cadmium-induced lipid peroxidation in multiple organs of rats. The investigation of OA on superoxide dismutase (SOD) activity showed that OA increased the SOD activity of cadmium-treated rat organs. More important, OA reduced the level of superoxide radical O²⁻ of cadmium-treated rat organs. And OA exhibited a strong DPPH radicals scavenging activity at dose of 10, 20 and 30 mg/mL, which may contributed to alleviating cadmium-induced oxidative stress. This study revealed that OA could significantly alleviate cadmium stress via reducing cadmium-induced lipid peroxidation and SOD activity inhibition through its radicals scavenging activity.