Abnormality of epiphyseal plate induced by selenium deficiency diet in two generation DA rats

This study aimed to observe the effects of Se deficiency on epiphyseal plates of two generation DA rats fed with artificial total synthetic low Se diet. All F0 and F1 DA rats were fed with synthetic low Se diet (SeD group) and low Se diet supplied with Se (SeS group). The levels of selenium and enzyme activities of GPx were detected in plasma of the rats. General growth of bone and articular cartilage was measured macroscopically and microscopically. The epiphyseal plate of femur heads or tibia were obtained to histological and immunohistochemical examinations. The cartilage from left knee joints and femur heads was used to detect the gene expression of collagens, ADAMTSs and several selenoproteins by RT‐qPCR. Two generation SeD rats showed Se insufficiency status. The thicknesses of the femur and tibial epiphyseal plates in both F0 and F1 SeD rats were significantly less than that of SeS rats. In F1 generation, SeD rats showed much fewer proliferative chondrocyte layers than SeS ones. Importantly, two generation SeD rats both showed significantly more serious pathological changes of epiphyseal plates. In two generation rats, gene expressions of COL II, GPx1 and GPx4 were significantly down‐regulated in SeD rats than SeS ones; meanwhile ADAMTS‐4 showed an up‐regulated expression in cartilage. Dietary Se deficiency can apparently cause epiphyseal plate lesion and decrease cartilage type II collagen production and GPx1 activity in two generation DA rats fed with the artificial total synthesis low Se diet.     

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

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

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

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

Pyrrolizidine alkaloid isoline-induced oxidative injury in various mouse tissues

Isoline is a retronecine-type pyrrolizidine alkaloid (PA) isolated from the traditional Chinese medicinal herb Ligularia duciformis. The present investigation was carried out to evaluate isoline-induced oxidative injury in various important mouse organs. Various tissue samples were collected after mice were administrated with 100 mg/kg isoline for 36 h, and then lipid peroxidation (LPO) level, total antioxidant capacity, glutathione-S-transferase (GST), glutathione peroxidase (GPx) and catalase (CAT) activities were determined to evaluate the oxidative injury. Our results showed that the total antioxidant capacity of liver, brain and lung were all decreased after given isoline, and the LPO level was increased in liver and heart of isoline-treated mice. Further antioxidant-related enzyme activity assays showed that isoline (100 mg/kg) decreased GPx activity in liver and heart, increased CAT activity in liver, brain and heart, and decreased the GST activity in lung. Taken together, our results demonstrate that isoline can induce different oxidative injury in various important mouse organs, and of which liver is the most sensitive organ.     

Early childhood wheezing symptoms in relation to plasma selenium in pregnant mothers and neonates

OBJECTIVE: Reduced dietary selenium intake has been linked to the development of asthma. We have investigated whether childhood wheezing symptoms, and asthma up to the age of 5 years are associated with plasma selenium and erythrocyte glutathione peroxidase (GPx) concentrations in pregnant mothers and neonates. METHODS: Two thousand pregnant women were recruited and their 1924 singleton children followed up. Plasma selenium and erythrocyte GPx concentrations were measured in maternal blood during early pregnancy (12 weeks gestation) and in neonatal cord blood. Cohort children were followed up at 1, 2 and 5 years using a respiratory symptom questionnaire and at 5 years children were also invited for spirometry and skin-prick test (SPT). Maternal and neonatal plasma selenium and erythrocyte GPx were related to the childhood outcomes of wheezing, and asthma. RESULTS: At 2 years 1282 children were followed up. At 5 years symptom data were available for 1167 children, 700 children were SPT tested, and forced expiratory volume in 1 s (FEV(1)) was measured in 478. Maternal plasma selenium concentration during early pregnancy was inversely associated with wheezing (odds ratio per 10 microg/kg plasma selenium 0.86, 95% confidence interval 0.76-0.97), and consulting a doctor because of wheeze (0.79, 0.69-0.93) in the second year of life. Cord plasma selenium was also inversely associated with wheezing (0.67, 0.47-0.96), and consulting a doctor because of wheeze (0.62, 0.41-0.93) in the second year of life. By age 5 these associations had disappeared. Maternal and neonatal erythrocyte GPx concentrations were not associated with any childhood outcomes at 2 or 5 years. CONCLUSION: The selenium status of mothers during early pregnancy, and neonates is associated with early childhood wheezing but not asthma or atopic sensitization, furthermore, this association is absent by the age of 5 years.     

Alpha-lipoic acid differently affects the reserpine-induced oxidative stress in the striatum and prefrontal cortex of rat brain

Antioxidative properties of alpha-lipoic acid (LA) are widely investigated in different in vivo and in vitro models. The aim of this study was to examine whether LA attenuates oxidative stress induced in rats by reserpine, a model substance frequently used to produce Parkinsonism in animals. Male Wistar rats were treated with reserpine (5 mg/kg) and LA (50 mg/kg) separately or in combination. The levels of reduced glutathione (GSH), glutathione disulfide (GSSG), nitric oxide (NO) and S-nitrosothiols as well as activities of glutathione peroxidase (GPx), glutathione-S-transferase (GST) and L-gamma-glutamyl transpeptidase (gamma-GT) were determined in the striatum and prefrontal cortex homogenates. In the striatum and prefrontal cortex a single dose of reserpine significantly enhanced levels of GSSG and NO but not that of S-nitrosothiols when compared with control. In the striatum, LA administered jointly with reserpine markedly increased the concentration of GSH and decreased GSSG level. In the prefrontal cortex, such treatment produced only an increasing tendency in GSH level but caused no changes in GSSG content. In both structures LA injected jointly with reserpine markedly decreased NO concentrations but did not cause significant changes in S-nitrosothiol levels when compared with control. Enzymatic activities of GPx and GST were intensified by LA in the striatum. In the prefrontal cortex, GPx activity was not altered, while that of GST was decreased. Gamma-GT activity was attenuated by reserpine in the striatum while LA reversed this effect. Such changes were not observed in the prefrontal cortex. The mode of LA action in the striatum during the reserpine-evoked oxidative stress strongly suggests that this compound may be of therapeutic value in the treatment of Parkinson's disease.     

Genetic toxicology testing of Di(2-ethylhexyl) terephthalate

Di(2-ethylhexyl) terephthalate (DEHT) is a commercially produced chemical (Kodaflex® DOTP) that is used as a general purpose, low-volatility plasticizer for polyvinyl chloride and other polymeric materials. Less than 30 million kilograms of DEHT are produced annually. DEHT is isomeric with di(2-ethylhexyl) phthalate (DEHP), a nongenotoxic rodent carcinogen whose mode of action has been suggested to derive from its ability to produce hepatocellular proliferation and/or hepatic peroxisome proliferation. Thus it is important to know the behavior of DEHT in genotoxicity assays in order to compare it with that of DEHP and other phthalate ester plasticizers. It is known from previously published studies that rats fed DEHT in the diet at 2,000 mg/kg produce urine that is negative in the Ames Salmonella bacterial mutagenicity assay in the presence and absence of induced rat liver S-9 and in the presence and obsence of β-glucuronidase/aryl sulfatase. Reported here are the results of direct testing of DEHT in the Ames plate incorporation assay, the Chinese hamster ovary/hypoxanthine guanine phosphoribosyl transferase (CHO/HGPRT) in vitro mammalian cell mutagenicity assay, and an in vitro chromosome aberrations assay using CHO cells. The results for mono(ethylhexyl) terephthalate (MEHT), a metabolite of DEHT, in the Ames Salmonella bacterial mutagenicity assay are also presented. All test results for both DEHT and MEHT were found to be negative, and it is therefore concluded that DEHT, like its isomeric relative DEHP, is not genotoxic. © 1994 Wiley-Liss, Inc.     

Effects of selenium on chromium (VI)-induced hepatotoxicity in adult rats

Chromium, a major environmental pollutant, is known for its wide toxic manifestations. The present experiment pertains to the protective role of selenium (Se) against K₂Cr₂O₇-induced hepatotoxicity. Female Wistar rats were divided into four groups of six each: group I served as controls which received standard diet; group II received in drinking water K₂Cr₂O₇ alone (700 ppm); group III received both K₂Cr₂O₇ and Se (0.5 Na₂SeO₃ mg/kg of diet); group IV received Se (0.5 mg/kg of diet) for 3 weeks. Exposure of rats to chromium promoted oxidative stress with an increase in malondialdehyde (MDA) and a decrease in glutathione (GSH) levels. A decrease in glutathione peroxidase (GPx) and an increase in superoxide dismutase (SOD) and catalase (CAT) activities were observed. Se supplementation to the diet of group III improved all the parameters cited above. Yet, plasma transaminases (AST and ALT), lactate dehydrogenase (LDH) activities, cholesterol, triglycerides (TG) and low density lipoprotein-cholesterol (LDL-C) levels increased, while high density lipoprotein-cholesterol (HDL-C) decreased. Co-administration of Se to the diet of group III restored hepatic markers to near-normal values. The biochemical results confirmed the histopathological findings. Therefore, our investigation revealed that Se was effective in preventing K₂Cr₂O₇-induced hepatotoxicity.     

Hepatoprotective role and antioxidant capacity of selenium on arsenic-induced liver injury in rats

The present study was undertaken to evaluate the protective effect of selenium against arsenic-induced oxidative damage in experimental rats. Males were randomly divided into four groups where the first was served as a control, whereas the remaining groups were respectively treated with sodium selenite (3 mg/kg b.w.), sodium arsenite (5.55 mg/kg b.w.) and a combination of sodium arsenite and sodium selenite. Changes in liver enzyme activities, thiobarbituric acid reactive substances (TBARS) level, antioxidants and reduced glutathione (GSH) contents were determined after 3 weeks experimental period.Exposure of rats to As caused a significant increase in liver TBARS compared to control, but the co-administration of Se was effective in reducing its level. The activities of glutathione peroxidase (GPx) and glutathione-S-transferase (GST) of As-treated group were found lower compared to the control and the Se-treated group. The co-administration of Se had an additive protective effect on liver enzyme activities compared to As-treated animals. On the other hand, a significant increase in plasmatic activities of AST, ALT and ALP was observed in As-treated group. The latter was also exhibited a decrease in body weight and an increase in liver weight compared to the control. The co-administration of Se has decreased the activities of AST, AST and ALP and improved the antioxidant status as well. Liver histological studies have confirmed the changes observed in biochemical parameters and proved the beneficial role of Se. To conclude, results suggest that As exposure enhanced an oxidative stress by disturbing the tissue antioxidant defense system, but the Se co-administration protected liver tissues against As intoxication probably owing to its antioxidant properties.     

低硒大鼠不同组织硒蛋白利用硒的优先性

硒（Ｓｅ）耗竭２０周的雄性Ｗｉｓｔａｒ大鼠分别饲以含硒为０．０１、０．０２、０．０５和０．２０ｍｇ／ｋｇ的四种饲料,于１、３、７、１４、２１和３５天时宰杀,动态观察不同组织中硒蛋白的变化,了解硒耗竭后补硒时组织及硒蛋白利用硒的优先性,由此推测它们的功能的相对重要性。结果表明硒蛋白利用硒的优先性顺序为硒蛋白Ｐ（Ｓｅ－Ｐ）、脱碘酶、磷脂氢谷胱甘肽过氧化物酶（ＰＨＧＰＸ）、细胞外谷胱甘肽过氧化物酶（ｅＧ     

Protective effect of date palm fruit extract (Phoenix dactylifera L.) on dimethoate induced-oxidative stress in rat liver

Nowadays, people’s exposure to chemical compounds such as organophosphorus insecticides is continuously on the rise more and more. Theses compounds have induced an excessive production of free radicals which are responsible for several cell alterations in the organism. Recent investigations have proved the crucial role of nutritional antioxidants to prevent the damage caused by toxic compounds. In this study, we investigate the role of date palm fruit extract (Phoenix dactylifera L.) in protection against oxidative damage and hepatotoxicity induced by subchronic exposure to dimethoate (20 mg/kg/day). Oral administration of dimethoate caused hepatotoxicity as monitored by the increase in the levels of hepatic markers enzymes (transaminases, alkaline phosphatase, gamma-glutamyl transferase and lactate dehydrogenase), as well as in hepatic malondialdehyde thus causing drastic alteration in antioxidant defence system. Particularly, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) were found increased by dimethoate while catalase (CAT) activity was reduced significantly. These biochemical alterations were accompanied by histological changes marked by appearance of vacuolization, necrosis, congestion, inflammation, and enlargement of sinusoids in liver section. Pretreatment with date palm fruit extract restored the liver damage induced by dimethoate, as revealed by inhibition of hepatic lipid peroxidation, amelioration of SOD, GPx and CAT activities and improvement of histopathology changes. The present findings indicate that in vivo date palm fruit may be useful for the prevention of oxidative stress induced hepatotoxicity.     

Methionine-supplemented diet augments hepatotoxicity and prooxidant status in chronically ethanol-treated rats

The purpose of this study was to investigate whether high methionine (HM) diet may influence the development of ethanol-induced hepatotoxicity and prooxidant–antioxidant balance in the liver. Rats received drinking water containing ethanol (20% v/v) and/or methionine supplemented diet (2% w/w) for 75 days. Although prooxidant–antioxidant balance did not change in the liver of rats in HM group, ethanol treatment was observed to increase plasma transaminase activities, and malondialdehyde (MDA) and protein carbonyl (PC) levels, but not glutathione (GSH), vitamin E and vitamin C levels, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities in the liver of rats as compared to controls. However, ethanol plus HM diet caused further increases in plasma transaminase activities and hepatic MDA and PC levels. In addition, SOD, GSH-Px and GST activities were observed to decrease, but GSH, vitamin E and vitamin C levels remained unchanged in the liver as compared to ethanol, HM and control groups. Our results show that HM diet may augment hepatotoxicity and oxidative stress in the liver of chronically ethanol-treated rats.     

The potential role of combined antioxidant treatment on pancreas of STZ-diabetic mice

In diabetes, cells and tissues are damaged due to the imbalance between production of free radicals and removal of them. The effective biologic antioxidants for oxidative stress such as α-lipoic acid, vitamin E and selenium are effective in diminishing oxidative damage such as membrane lipid peroxidation. The experiment aimed to investigate the oxidative stress occurring in mitochondrial and cytoplasmic fraction of pancreatic tissues in streptozotocin-diabetic mice and the possible effects of α-lipoic acid + vitamin E + selenium combination on oxidative damage and antioxidative system by using microscopic and biochemical methods.The mice were divided into five groups. These groups were treated by citrate buffer, the solvents of the antioxidants, combined the antioxidants [α-lipoic acid (50 mg/kg), vitamin E (100 mg/kg), selenium (0.25 mg/kg)], streptozotocin (40 mg/kg × 5), combined the antioxidants and streptozotocin. The mice were sacrificed by cervical dislocation.In the experimental group given combined antioxidants following results were observed compared to diabetic group: increased percent insulin-positive cell area; decreased blood glucose levels; increased manganase superoxide dismutase activities and unsignificantly increased superoxide dismutase activities; unsignificantly decreased lipid peroxidase levels in both of fraction; unsignificantly decreased in mitochondrial fraction and unsignificantly increased in cytosolic fraction for catalase levels; not any alteration glutathione levels; not any activity in both of fraction for glutathione peroxidase.We can say that by taking the blood glucose levels and immunohistochemical results into account, the combination of triple antioxidants has a partly positive effect on diabetes. This positive effect could increase when trying different doses of combined antioxidant treatment.     

Hepatoprotection with a chloroform extract of Launaea procumbens against CCl4-induced injuries in rats

ABSTRACT: BACKGROUND: Launaea procumbens (Asteraceae) is used as a folk medicine to treat hepatic disorders in Pakistan. The effect of a chloroform extract of Launaea procumbens (LPCE) was evaluated against carbon-tetrachloride (CCl4)-induced liver damage in rats. METHODS: To evaluate the hepatoprotective effects of LPCE, 36 male Sprague-Dawley rats were equally divided into six groups. Animals of group 1 (control) had free access to food and water. Group II received 3 ml/kg of CCl4 (30% in olive oil v/v) via the intraperitoneal route twice a week for 4 weeks. Group III received 1 ml of silymarin via gavage (100 mg/kg b.w.) after 48 h of CCl4 treatment whereas groups IV and V were given 1 ml of LPCE (100 and 200 mg/kg b.w., respectively) after 48 h of CCl4 treatment. Group VI received 1 ml of LPCE (200 mg/kg b.w.) twice a week for 4 weeks. The activities of the antioxidant enzymes catalase, peroxidase (POD), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), glutathione reductase (GSR), glutathione (GSH) and lipid peroxidation (thiobarbituric acid reactive substances (TBARS)) were measured in liver homogenates. DNA damage, argyrophilic nucleolar organizer regions (AgNORs) counts and histopathology were studied in liver samples. Serum was analyzed for various biochemical parameters. Phytochemical composition in LPCE was determined through high-performance liquid chromatography (HPLC). RESULTS: LPCE inhibited lipid peroxidation, and reduced the activities of aspartate transaminase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase in serum induced by CCl4. GSH contents were increased as were the activities of antioxidant enzymes (catalase, SOD, GST, GSR, GSH-Px) when altered due to CCl4 hepatotoxicity. Similarly, absolute liver weight, relative liver weight and the number of hepatic lesions were reduced with co-administration of LPCE. Phyochemical analyses of LPCE indicated that it contained catechin, kaempferol, rutin, hyperoside and myricetin. CONCLUSION: These results indicated that Launaea procumbens efficiently protected against the hepatotoxicity induced by CCl4 in rats, possibly through the antioxidant effects of flavonoids present in LPCE. KEYWORDS: Launaea procumbens, hepatic injuries, flavonoids, antioxidant enzymes, carbon tetrachloride.     

Ethanol induced adaptive changes in blood for the pathological and toxicological effects of chronic ethanol consumption in humans

Alcohol consumption is associated with a number of toxicological changes in blood and the oxidant–antioxidant system. The present study was performed to investigate the alcohol induced toxicological, pathological changes in blood and an adaptive role of erythrocyte antioxidant system in chronic alcoholics. Human male volunteers aged 44 ± 6 years with similar dietary habits were divided into two groups, namely non-alcoholic controls and chronic alcoholics. We measured hematological parameters, erythrocyte lipid peroxidation, NO production, erythrocyte antioxidant and liver function test enzyme activities. Alcoholics had increased erythrocyte nitric oxide levels and also elevated erythrocyte lipid malondialdehyde (MDA) concentrations. Strikingly, increments in reduced glutathione and markedly increased activities of certain antioxidant enzymes such as glutathione reductase (GR), superoxide dismutase (SOD), and another related enzyme G-6 phosphate dehydrogenase (G6-PDH) with no alterations in the activities of glutathione S-transferase (GST), glutathione peroxidase (GPx), and catalase (CAT) in chronic alcoholics were observed compared to controls. Furthermore, erythrocyte NO levels were positively correlated with lipid peroxidation, SOD, GSH, GR and G6PDH in chronic alcoholics. In addition, increased AST/ALT ratio and a significant increase in WBC and platelets were also noticed. Together, these results indicate that, antioxidants and defense enzymes appear to be rendering protection as a consequence of chronic adaptation in alcoholics.     

Effect of caffeic acid derivatives on polychlorinated biphenyls induced hepatotoxicity in male mice

Chronic exposure to coplanar polychlorinated biphenyls（PCBs）,a potent inducer of toxic reactive oxygen species（ROS）,in the environment and food can cause liver diseases.It remains unknown whether caffeic acid derivatives（CADs） exerted protective effect on PCB-induced hepatotoxicity.We sought to evaluate the activities of 3CADs on PCB169-induced oxidative stress and DNA damage in the liver.Male ICR mice were administered with1 μmol/mL PCB169 at 5 mL/kg body weight for 2 weeks.The mice were given CADs by gastric gavage for 3weeks.We found that PCB169 decreased the growth rate and reduced the levels of superoxide dismutase（SOD）,glutathione（GSH） and GSH peroxidase（GPx）.It increased the liver weight,malondialdehyde（MDA）and 8-hydroxy-2＇-deoxyguanosine（8-OHdG） levels and CYPlAl activity in the liver tissues and plasma of mice（P〈0.05）.Pretreatment of mice with CADs restored the above parameters to normal levels.There was a synergistic protective effect between CADs in preventing MDA and 8-OHdG formation and inducing CYPlAl and phase II metabolism enzyme（SOD,GPx） activities（P〈0.05）.In conclusion,PCB169 induced hepatotoxicity and pretreatment with CADs had synergistic protective effects on liver damage.     

Effect of Zingiber officinale on liver oxidative status and biochemical parameters in rats exposed to paraquat

Oxidative stress caused by reactive oxygen species is one of the major pathogenesis of important diseases of animals and human. Paraquat is widely used as herbicide. The toxicity of paraquat is through induction of oxidative processes in biological systems. Biochemically, this herbicide interferes with intracellular electron transfer system leading to the formation of superoxide anion. Zingiber officinale (ginger) is widely used as a spice and medical treatment for various diseases. The objective of this study was to assess the effect of different levels of ginger extract on antioxidant status and serum metabolites of rats. Sixty male albino Wistar rats were divided in six groups as follows: control (saline); ginger; paraquat; paraquat with 100, 200, and 400 ginger. After 30 days of treatment, the blood was collected by cardiac puncture. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), reduced glutathione (GSH), and lipid peroxidation were estimated. In paraquat-treated group, the serum levels of ALT, AST, and malondialdehyde (MDA) were markedly raised. Administration of ginger extract with paraquat reduced the serum levels of ALT, AST, and MDA. Hepatic SOD, CAT, GPx, GST, and GSH activities were significantly decreased in paraquat-treated group compared to those of control. However, concurrent administration of paraquat with all concentrations of ginger extract had the opposite effect, where it increased the hepatic SOD, CAT, GPx, GST, and GSH activities near to control. The present study demonstrates that administration of ginger extract to rats modulates the antioxidant enzymes and suggests a possible adaptive mechanism to counteract oxidative stress situation.     

Antioxidant enzyme immunoreactivity in rat von Ebner gland after nickel treatment

Our study was designed to clarify the role of antioxidant enzymes in the rat von Ebner gland during acute nickel toxicity. After treatment with nickel acetate, we monitored ultrastructural alterations in acinar and ductal cells, immunohistochemical staining for glutathione peroxidase (GPx) and glutathione S-transferases (GST mu and GST pi), and immunoreactivity for malondialdehyde (MDA). Immunoreactivity for MDA was present only in the acinar cells, and it was enhanced at 3 h after Ni treatment. In contrast, immunoreactivities for GPx and GSTs did not change in acinar cells but significantly increased in ductal cells after Ni treatment. Cytoplasmic vacuoles increased in acinar cells at 3 h after Ni treatment, but they almost completely disappeared at 24 h. No morphological changes were observed in taste bud cells from Ni-treated rats. Because lipid peroxidation, as monitored by immunoreactivity for MDA, was only transiently increased in the acinar cells, the enhanced antioxidant enzyme immunoreactivity in ductal cells of the von Ebner gland plays a crucial role in the self-defense system against nickel toxicity in the rat oral cavity.     

Selenium provides protection to the liver but not the reproductive organs in an atrazine-model of experimental toxicity

The present study evaluated the possible protective effects of selenium against atrazine-induced toxicity in the liver and reproductive system of rats. Atrazine administered to rats orally at a dose of 120 mg/kg caused an inhibition in the activity of glutathione-S-transferase and an increase in malondialdehyde formation in the liver, testis and epididymis. Superoxide dismutase decreased in the liver and testis but was increased in the epididymis. Furthermore, hepatic glutathione and lactate dehydrogenase activity increased while epididymal catalase, ascorbate content, hepatic aspartate aminotransferase and glutathione peroxidase activities in all the tissues decreased in the atrazine-treated animals. Hepatic, testicular and epididymal alanine aminotransferase activities were not affected by atrazine (p>0.05). Decreased epididymal and testicular sperm number, sperm motility, daily sperm production and increased number of dead and abnormal sperm were observed in atrazine-treated rats.Treatment of rats orally with selenium at a dose of 0.25 mg/kg did not prevent atrazine-induced changes in sperm characteristics and had no protective effects against atrazine-induced biochemical alterations in the testis and epididymis except testicular lactate dehydrogenase. Catalase activity and ascorbate contents were unchanged in these groups of animals. However, selenium effectively protected against atrazine-induced changes in biochemical indices in the liver. In rats treated with selenium alone, glutathione peroxidase in all the tissues, hepatic glutathione and superoxide dismutase, testicular lactate dehydrogenase activity and ascorbate content increased, while hepatic catalase activities decreased (p<0.05).Our data suggest that selenium effectively attenuated the toxic effects of atrazine-induced liver changes but not in the reproductive organs and sperms of rats. Selenium might therefore be useful in ameliorating oxidative stress in the liver.