Oxidative stress in heart tissue of hyperthyroid and iron supplemented rats.

This study was designed to investigate the effect of hyperthyroidism and/or iron supplementation or cardiac oxidative stress parameters--the lipid peroxidation end product glutathione (GSH), glutathione peroxidase (CSH-Px), and superoxide dismutase (CuZnSOD)--in rats. In plasma, ferritin as an indicator of iron status and glutamate oxaloacetate transaminase (GOT) as an indicator of damage to the heart tissue were analyzed. Our findings show that hyperthyroidism increased lipooxidative damage as reflected by higher lipid peroxidation end product levels and elevated antioxidant defense parameters-GSH and GSH-Px. Iron supplementation per se does not affect oxidative stress parameters studied in the euthyroid state. Although iron increased lipid peroxidation in the hyperthyroid state, this effect was less than that seen in euthyroidism. Iron supplementation to hyperthyroid rats significantly lowered plasma ferritin levels, suggesting increased iron elimination with consequently reduced oxidative stress.     

Effect of l-ascorbic acid on antioxidant defense system in testes of albino rats exposed to nickel sulfate

We studied the effect of oral supplementation with L-ascorbic acid (50 mg/100 g body weight) on nickel sulfate (2.0 mg/100 g body weight, i.p.) induced lipid peroxidation in the testes of Wister strain male albino rats. Testicular lipid peroxide and glutathione (GSH) levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated. Nickel sulfate treatment significantly increased the level of testicular lipid peroxide and decreased all antioxidant enzymes activities and GSH concentration. Simultaneously treatment of L-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on testicular lipid peroxide and GSH concentration as well as antioxidant enzymatic defense system.     

Attenuation of oxidative stress in plasma and tissues of rats with experimentally induced hyperthyroidism by caffeic acid phenylethyl ester

Increased oxidative stress with high free radical generation has been described previously in animal models of hyperthyroidism. The present study was designed to investigate the protective effects of caffeic acid phenylethyl ester (CAPE) on oxidative damage in rats with experimentally induced hyperthyroidism. The study was conducted on 32 male Sprague-Dawley rats. The experimental animals were divided into four groups (control, CAPE alone, hyperthyroidism, and hyperthyroidism + CAPE). Hyperthyroidism was induced by intraperitoneal administration of 0.3 mg/kg/day L-thyroxine for 4 weeks. CAPE (10 micro g/kg) was administered intraperitoneally for 4 weeks. At the end of the experimental period, blood samples and various organs (liver, heart and brain) of rats were taken for the determination of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), oxidized glutathione, vitamin C and superoxide dismutase (SOD) levels and concentrations of triiodothyronine (T3), thyroxine (T4) and thyroxine-stimulating hormone (TSH). Our results indicate that TBARS, oxidized glutathione, SOD levels and concentrations of T3 and T4 were higher in plasma and tissues of the hyperthyroid group compared to controls. Vitamin C, GSH and TSH levels were decreased significantly in the hyperthyroid group when compared to the control group. CAPE treatment decreased the elevated TBARS, SOD, T3 and T4 levels and increased the lowered GSH, vitamin C and TSH levels to control levels in rats with hyperthyroidism. In conclusion, our results indicate that CAPE is beneficial as a protective agent against oxidative stress induced by hyperthyroidism in rats. The protection is probably due to multiple mechanisms involving free radical scavenger properties, attenuating lipid peroxidation and increasing the antioxidant status.     

Changes in antioxidant defense systems induced by thiram in V79 Chinese hamster fibroblasts.

The role of antioxidant defence systems in protection against oxidative damage of lipids and proteins induced by fungicide thiram during in vitro exposure was investigated in cultured Chinese hamster V79 cells with normal, depleted, and elevated glutathione (GSH) levels. We analyzed the catalytic activities of superoxide dismutases (SOD1 and SOD2), Se-dependent and Se-independent glutathione peroxidases (GSH-Px), glutathione reductase (GR), and catalase (CAT), as well as total glutathione/glutathione disulfide ratio (GSH(total)/GSSG). Thiram treatment resulted in an increase in activities of SOD1, Se-dependent GSH-Px, and GR at the highest tested dose (150 microM). On the contrary, inhibition of CAT and Se-independent GSH-Px activities, and no significant changes in the level of SOD2 activity was observed at any tested doses (100-150 microM). GSH(total)/GSSG ratio in the 100 microM thiram treated cells was not significantly changed comparing to the control, despite significant decrease of GSH total (50%). In 150 microM thiram treated cells the ratio falls to 43% of control value. Pretreatment with l-buthionine sulfoximine (L-BSO), an inhibitor of GSH synthesis, significantly enhanced decrease in CAT and Se-independent GSH-Px activities, as well as GSH(total)/GSSG ratio, and reduced Se-dependent GSH-Px activity, following exposure to thiram. Simultaneously, L-BSO pretreatment enhanced increase in SOD1 activity, and had no effect on SOD2, following thiram exposure. Pretreatment with N-acetyl cysteine (NAC), a GSH precursor, prevented enzymatic changes in CAT, Se-dependent GSH-Px, GR, SOD1 activities, and significantly decreased SOD2 activity following exposure to thiram. GSH(total)/GSSG ratio was restored to the control value. This study suggests that following the changes in antioxidant defense systems thiram can act through the production of free radicals.     

Effect of alpha-tocopherol on the cardiac antioxidant defense system and atherogenic lipids in cigarette smoke-inhaling mice

The present study was designed to evaluate the role of alpha-tocopherol (AT) on the cardiac antioxidant defense system and atherogenic lipid profile in cigarette smoke (CS)-inhaling mice. CS exposure for 10 wk resulted in an increase in the levels of lipid peroxidation (LPO) and reduction in reduced glutathione (GSH) levels in heart. Supplementation with AT reduced LPO and restored GSH levels to almost those of normals. The activities of the antioxidant enzymes catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) increased after CS inhalation. However, supplementation with AT resulted in reversing the increase in GSH-Px and GR. The activity of superoxide dismutase (SOD) remained unaltered in all the groups studied. Levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) increased, whereas high-density lipoprotein cholesterol (HDL-C) levels decreased in serum following CS inhalation. Supplementation with AT reduced the levels of LDL-C and TG. On the other hand, AT-fed animals showed an increase in HDL-C levels on CS exposure. Based on the results it appears that AT protects the heart from CS-induced peroxidative damage and has antiatherogenic properties.     

Lipid peroxidation and antioxidants in plasma and red blood cells from patients with pemphigus vulgaris

In pemphigus vulgaris, the increased production of reactive oxygen species from activated neutrophils decreases concentrations of antioxidant vitamins and enzymes in plasma and red blood cells (RBC), resulting in oxidative stress. We compared lipid peroxidation, a measure of reactive oxygen species production, antioxidant vitamins, reduced glutathione (GSH), glutathione peroxide (GSH-Px), and catalase enzyme activity in blood samples obtained from 18 nonsmoking pemphigus vulgaris patients and an equal number of age- and gender-matched, healthy control subjects. Plasma and RBC lipid peroxidation levels (malonyl dialdehyde) were significantly higher (p < 0.05) in pemphigus vulgaris patients than in control subjects. Significantly lower concentrations of plasma antioxidant vitamins (vitamin E and beta-carotene) and vitamin A (p < 0.001), antioxidant enzymes (catalase in RBC and plasma, GSH-Px in RBC [p < 0.05]), and respective GSH activities in both RBC and plasma (p < 0.05 and p < 0.01) were found in pemphigus vulgaris patients than in control subjects. GSH-Px in plasma did not change significantly. The results provide evidence for a potential role of increased lipid peroxidation and peroxidation and decreased antioxidants in pemphigus vulgaris by its inflammatory character.     

Protective effects of L-arginine on pulmonary oxidative stress and antioxidant defenses during exhaustive exercise in rats

AIM: To assess the effects of L-arginine (L-Arg) supplementation on pulmonary oxidative stress and antioxidant defenses in rats after exhaustive exercise. METHODS: Rats were randomly divided into four groups: sedentary control (SC), sedentary control with L-Arg treatment (SC+Arg), exhaustive exercise with control diet (E) and exhaustive exercise with L-Arg treatment (E+Arg). Rats in groups SC+Arg and E+Arg received a 2% L-Arg diet. Rats in groups E and E+Arg underwent an exhaustive running test on a motorized treadmill. Pulmonary oxidative stress indices [xanthine oxidase (XO), myeloperoxidase (MPO), and malondialdehyde (MDA)] and antioxidant defense systems [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and glutathione (GSH)] were investigated in this study. RESULTS: L-Arg supplementation significantly reduced exercise-induced elevations of XO and MPO activities in lung. L-Arg reversed the exercise-induced increase in SOD and GR activities, but increased CAT and GPX activities. L-Arg administration also significantly increased the GSH levels in plasma. CONCLUSION: L-Arg supplementation can prevent elevations of XO and MPO activities in the lung and favorably influence pulmonary antioxidant defense systems after exhaustive exercise.     

Diallyl trisulfide (DATS) effectively attenuated oxidative stress-mediated liver injury and hepatic mitochondrial dysfunction in acute ethanol-exposed mice

The protective effects of diallyl trisulfide (DATS) on acute ethanol-induced liver injury were investigated. Mice were pretreated with DATS (30mg/kgbw) for 7d before being exposed to ethanol (4.8g/kgbw). The biochemical indices (aspartate amino transferase, AST; alanine amino transferase, ALT; triglyceride, TG) were examined to evaluate the protective effects. Mitochondria were isolated for the mitochondrial permeability transition (MPT), membrane potential (DeltaPsi(m)) and adenosine nucleotide pool assay. The lipid peroxidation (malondialdehyde, MDA), non-enzymatic antioxidant (glutathione, GSH) and enzymatic antioxidants (superoxide dismutase, SOD; catalase, CAT; glutathione reductase, GR; glutathione peroxidase, GSH-Px) were measured both in the liver homogenate and isolated mitochondria. Acute ethanol exposure resulted in the significant increase of the ALT, AST and TG levels and hepatic mitochondria dysfunction shown as MPT, and the decreases of DeltaPsi(m), ATP and energy charge (EC). However, DATS pretreatment dramatically attenuated these adverse effects. Beside this, DATS was found to significantly inhibit the increase of the hepatic and mitochondrial MDA levels, which were decreased by 33.3% (P<0.01) and 39.0% (P<0.01), respectively. In addition, DATS pretreatment markedly suppressed the ethanol-induced decrease of the hepatic GSH level and increased the mitochondrial GSH level. Moreover, the activities of the hepatic antioxidant enzymes (SOD, CAT, and GR) and the mitochondrial antioxidant enzymes (SOD, GR, and GSH-Px) were significantly boosted. Thus, we concluded that DATS dramatically attenuated acute ethanol-induced liver injury and mitochondrial dysfunction. The increase of the hepatic and mitochondrial GSH levels and the elevation of the antioxidant enzymes activities should account for the preventive effects.     

The protective role of ferulic acid on sepsis-induced oxidative damage in Wistar albino rats

Oxidative stress has an important role in the development of sepsis-induced multiorgan failure. Ferulic acid (FA), a well-established natural antioxidant, has several pharmacological activities including anti-inflammatory, anticancer and hepatoprotective. This study aimed to investigate the effects of FA on sepsis-induced oxidative damage in Wistar albino rats. Sepsis-induced DNA damage in the lymphocytes, liver and kidney cells of rats were evaluated by comet assay with and without formamidopyrimidine DNA glycosylase (Fpg). The oxidative stress parameters such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and total glutathione (GSH) and malondialdehyde (MDA) levels were also measured. It is found that DNA damage in sepsis + FA-treated group was significantly lower than the sepsis group. FA treatment also decreased the MDA levels and increased the GSH levels and SOD and GSH-Px activities in the sepsis-induced rats. It seems that FA might have ameliorative effects against sepsis-induced oxidative damage.     

Effect of α-Tocopherol on the Cardiac Antioxidant Defense System and Atherogenic Lipids in Cigarette Smoke-Inhaling Mice

The present study was designed to evaluate the role ofα -tocopherol (AT) on the cardiac antioxidant defense system and atherogenic lipid profile in cigarette smoke (CS)-inhaling mice. CS exposure for 10 wk resulted in an increase in the levels of lipid peroxidation (LPO) and reduction in reduced glutathione (GSH) levels in heart. Supplementation with AT reduced LPO and restored GSH levels to almost those of normals. The activities of the antioxidant enzymes catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) increased after CS inhalation. However, supplementation with AT resulted in reversing the increase in GSH-Px and GR. The activity of superoxide dismutase (SOD) remained unaltered in all the groups studied. Levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) increased, whereas high-density lipoprotein cholesterol (HDL-C) levels decreased in serum following CS inhalation. Supplementation with AT reduced the levels of LDL-C and TG. On the other hand, AT-fed animals showed an increase in HDL-C levels on CS exposure. Based on the results it appears that AT protects the heart from CS-induced peroxidative damage and has antiatherogenic properties.     

Effect of exercise training on antioxidant system in brain regions of rat

The purpose of this investigation was to determine whether any alterations in antioxidant enzyme activities and levels of glutathione (GSH) in brain regions occurred following exercise training. Sprague-Dawley rats were given exercise training on a treadmill for 7.5 weeks and sacrificed 18 h after the last exercise along with the sedentary control rats. Different brain regions—cerebral cortex (CC), brainstem (BS), corpus striatum (CS), and hippocampus (H)—were isolated; GSH, oxidized glutathione (GSSG), Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined. The exercise training increased SOD activity significantly (130% of sedentary control) in BS and in CS. SOD activity in H was the lowest of all four brain regions. Different brain regions showed GSH-Px activity in decreasing order for CS < BS < CC < H. GSH levels were 43% less in BS than CC and CS. The ratio of GSH/ GSSG significantly increased from 6.8 to 8.3 in CC, and from 9.4 to 13.5 in BS as a result of exercise training. Different brain regions contained different activities of antioxidant enzymes, as well as GSH and GSSG levels, which were preferentially altered as a result of exercise training to cope with oxidative stress.     

LIPID PEROXIDATION AND ANTIOXIDANT STATUS IN THE LIVER,ERYTHROCYTES, AND SERUM OF RATS AFTER METHANOL INTOXICATION

Lipid peroxidation products measured as a malondialdehyde and activities of superoxide dism utase (SOD), glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), and concentrations of ascorbic acid,-tocopherol, and glutathione (GSH) were measured in the liver, erythrocytes, and serum of rats 6, 14, and 24 h and 2, 5, and 7 d after treatment with 3 g methanol/ kg. GSH-Px and GSSG-R activities, GSH level, and ascorbate concentration in the liver, erythrocytes, and blood serum were significantly decreased. In addition, SOD and-tocopherol in erythrocytes were diminished, while malondialdehyde (MDA) in liver, erythrocytes, and serum were elevated. Further, erythrocyte counts, hemoglobin levels, hematocrit, and mean corpuscular volume (MCV) were reduced. These results indicate that methanol intoxication in rats leads to an increase in the lipid peroxidation and impairment in the antioxidant mechanisms in liver, erythrocytes, and blood serum.     

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.     

Effects of Dietary Ferulic Acid Supplementation on Hepatic Injuries in Tianfu Broilers Challenged with Lipopolysaccharide

Lipopolysaccharide (LPS) is an endotoxin that can cause an imbalance between the oxidation and antioxidant defense systems and then induces hepatic damages. Ferulic acid (FA) has multiple biological functions including antibacterial and antioxidant activities; however, the effect of FA on lipopolysaccharide-induced hepatic injury remains unknown. The purpose of this study was to investigate the mechanism of action of dietary Ferulic acid against Lipopolysaccharide-induced hepatic injuries in Tianfu broiler chickens. The results showed that supplementation of FA in daily feed increased body weight (BW) and decreased the feed conversion ratio (FCR) in LPS treatment broilers significantly (p < 0.05). Additionally, supplement of FA alleviated histological changes and apoptosis of hepatocytes in LPS treatment broilers. Supplement of FA significantly decreases the activities of ROS. Interestingly, the levels of antioxidant parameters including total superoxide dismutase (T-SOD), total antioxidant capacity (T-AOC), and glutathione (GSH) in LPS group were significantly increased by the FA supplementation (p < 0.05). Nevertheless, administration of LPS to broilers decreased the expressions of Nrf2, NQO1, SOD, GSH-Px, CAT and Bcl-2, whereas it increased the expressions of Bax and Caspase-3 (p < 0.05). Moreover, the expressions of Nrf2, NQO1, SOD, CAT, Bcl-2 were significantly upregulated and Caspase-3 were significantly downregulated in the FL group when compared to LPS group (p < 0.05). In conclusion, supplementation of FA in daily feed improves growth performance and alleviates LPS-induced oxidative stress, histopathologic changes, and apoptosis of hepatocytes in Tianfu broilers.     

Effect of cigarette smoke inhalation on antioxidant enzymes and lipid peroxidation in the rat

Inhalation of cigarette smoke significantly increased glutathione (GSH) content and increased lipid peroxidation without altering the activities of Superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px) or glutathione reductase (GR) in the lung (six male Wistar rats). Following intratracheal administration of benzo[a]pyrene (BP), an increase in pulmonary GSH-Px activity, GSH content and lipid peroxidation was observed after 12 h. GSH-Px activity and GSH content returned to control values by 7 and 30 days, respectively, whereas lipid peroxidation in the lung remained significantly greater than the control value for up to 7 days of BP administration. Hepatic activity of SOD was increased significantly, whereas the activities of GSH-Px, catalase, GR, and GSH content were not changed by inhalation of cigarette smoke. On administration of BP, a significant increase in the activities of SOD and GSH-Px was observed at 12 h. After 7 and 30 days, the activities of these antioxidant enzymes were comparable to their respective control group values. No change in the activity of catalase or in the level of lipid peroxidation was noted throughout the entire study period.     

糖尿病大鼠肾脏抗氧化防御系统机能的改变

目的：探讨糖尿病对肾脏抗氧化防御机能的影响。方法：观察12周糖尿病大鼠肾皮质丙二醛(MDA)及谷胱甘肽(GSH)水平,以及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、谷胱甘肽S转移酶(GSH-ST)和过氧化氢酶(CAT)活性的变化。结果：糖尿病大鼠肾组织中SOD、CAT活性下降;GSH含量显著降低;MDA没有变化;GSH-PX活性却明显增强。结论：糖尿病大鼠肾组织抗氧化防御机能明显下降。     

Influence of Indole-3-butyric acid on antioxidant defense systems in various tissues of rats at subacute and subchronic exposure

This study was carried out to investigate the effects of Indole-3-butyric acid (IBA), a plant growth regulator (PGR), on antioxidant defense systems (ADS) such as reduced glutathione (GSH) level and Glutathione-S-transferase (GST), glutathione peroxidase (GSH-Px) superoxide dismutase (SOD) enzymes activity in various tissues of rats exposed to 25 and 50 ppm dosages of IBA for 20 and 45 days. Results showed that the administrations of IBA fluctuated GSH levels in some tissues of rats treated with both dosages and periods. With regard to the ADS enzymes, SOD and GST activities increased significantly in the most of the tissues in rats treated with both dosages and periods of IBA. Also, GSH-Px activity fluctuated after subacute and subchronic exposure with both dosages in some of the tissues in rats compared to that the control rats. The observations presented led us to conclude that the administrations of IBA at subacute and subchronic affected the ADS system in various tissues of rats. This may reflect the potential role of these parameters as useful biomarkers for toxicity of IBA.     

Serum and intraerythrocyte antioxidant enzymes and lipid peroxides in children with migraine

The oxidant-antioxidant balance disorders underlie a number of acute and chronic diseases of the central nervous system (CNS). It is believed that oxidative stress plays a role in the pathogenesis of migraine. The study objective was to assess the processes of lipid peroxidation with malondialdehyde (MDA) as its major indicator and to determine the activities of antioxidant enzymes: superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione reductase (GSSG-R) in the serum and erythrocytes of patients at developmental age with migraine with and without aura. The study group consisted of 34 patients at the age of 10-18 years (mean +/- standard deviation: 14.04 +/- 2.29 years), suffering from migraine. The control group included 38 patients, aged 4-17 years (mean age 12.11 +/- 3.46). MDA concentration and activities of SOD, GSH-Px and GSSG-R were determined in serum and erythrocytes of all the patients. In the migraine group, the MDA levels in serum and erythrocytes were statistically significantly lower than in control subjects (p < 0.001). In the migraine group, serum GSH-Px activity was significantly higher (p < 0.05). The GSSG-R activity in the erythrocytes of migraine children was significantly higher compared to controls (p < 0.001). SOD activity was decreased and GSH-Px was increased (non-significantly) in erythrocytes of migraineurs. Our results confirm the disturbances of lipid peroxidation processes in migraine and suggest the activation of antioxidant mechanisms. Its important indicator seems to be the increase in the GSSG-R activity in the erythrocytes and the GSH-Px activity in serum between migraine attacks. Further studies are necessary.     

Methiocarb-induced oxidative damage following subacute exposure and the protective effects of vitamin E and taurine in rats

Methiocarb, is used worldwide in agriculture and health programs. Besides its advantages in the agriculture, it causes several toxic effects. In this study, we aimed to investigate subacute effects of methiocarb on lipid peroxidation, reduced glutathione (GSH), antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) and histopathological changes in rat tissues. Moreover, we examined the possible protective effects of vitamin E and taurine on methiocarb-induced oxidative damage in rat tissues. Rats were randomly divided into six groups as follows; I-control group; II-methiocarb group; III-vitamin E group; IV-vitamin E + methiocarb group; V-taurine group and VI-taurine + methiocarb group. Methiocarb significantly increased lipid peroxidation in liver and kidney when compared to control groups. Levels of GSH and activities of SOD, CAT and GSH-Px were found to be decreased, while GSH-Rd remained unchanged in rat liver and kidney treated with methiocarb. Pretreatment of vitamin E and taurine resulted in a significant decrease on lipid peroxidation, alleviating effects on GSH and antioxidant enzymes. The degenerative histological changes were less in liver than kidney of rats treated with methiocarb. Pretreatment of vitamin E and taurine showed a protective effect on the histological changes in kidney comparing to the liver of rats treated with methiocarb.     

Efficacy of the potential chemopreventive agent, hesperetin (citrus flavanone), on 1,2-dimethylhydrazine induced colon carcinogenesis

Our current study is an effort to identify a potent chemopreventive agent against colon cancer. Here we have investigated the efficacy of hesperetin on tissue lipid peroxidation, antioxidant defense system and colonic histoarchitecture in male Wistar rats in colon carcinogenesis. Rats in groups 3, 4, 5 and 6 were treated with DMH (20 mg kg body weight s.c.) once a week for 15 weeks. Group 1 rats received modified pellet diet and served as control; group 2 received modified pellet diet along with hesperetin (20 mg/kg body weight, p.o., every day); and hesperetin was given to the rats as in-group 2 during the initiation, post-initiation and entire period stages of colon carcinogenesis. Lipid peroxidation was studied by measuring the formation of thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD), and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), reduced glutathione (GSH), in the liver and colonic tissues of DMH administered rats. (1) Decreased levels of lipid peroxidation in the colonic tissues; (2) decreased activities of antioxidant enzymes SOD, CAT, GPX, GR and GSH levels in the tissues on DMH treatment. Hesperetin supplementation during the initiation, post-initiation and entire period stages of carcinogenesis significantly reversed these activities. These results indicate that hesperetin may be a potential chemopreventive agent against DMH-induced colon cancer.