Ameliorative role of conjugated linolenic acid isomers against oxidative DNA damage induced by sodium arsenite in rat model

The present study was undertaken to evaluate the ameliorative role of α-eleostearic acid and punicic acid, isomers of conjugated linolenic (CLnA) acid, against oxidative stress induced DNA damage. Male albino rats were divided into six groups. Group 1 and 2 were normal control and sodium arsenite treated (Sa; 10 mg/kg BW) control respectively. Group 3–6 were orally treated with different doses of two fatty acids (0.5% and 1.0% of total lipid given for each isomer) along with sodium arsenite (Sa; 10 mg/kg BW). Comet assay of blood leukocytes showed that administration of CLnA reduced DNA damage significantly (P < 0.05) which was determined by tail DNA percent and olive tail moment. Results showed that activity of antioxidant enzymes viz. catalase, superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH) in plasma, liver and erythrocyte lysate decreased and activity of nitric oxide synthase in plasma and liver increased significantly due to oxidative stress generated by sodium arsenite. Administration of CLnA isomers restored all the altered parameters and also reduced lipid peroxidation and leakage of transaminase enzymes from liver to blood due to liver injury. α-Eleostearic acid was more efficient antioxidant than punicic acid against oxidative DNA damage.     

Prophylactic effect of α-linolenic acid and α-eleostearic acid against MeHg induced oxidative stress,DNA damage and structural changes in RBC membrane

The present study was undertaken to evaluate under in vivo condition the effects of α-linolenic acid and α-eleostearic acid against methyl mercury (MeHg) induced oxidative stress. Male albino rats were divided into six groups. Group 1 was under normal control and Group 2 was treated with methyl mercury chloride (MeHgCl; 5 mg/kg BW/day). Groups 3, 4, 5 and 6 were orally treated with different doses of the two fatty acids (0.5% and 1.0% of total lipid given for each kind of linolenic acid isomer) along with MeHgCl (5 mg/kg BW). Comet assay of blood lymphocytes showed that administration of α-linolenic acid reduced DNA damage significantly (P < 0.05). Results also showed that activity of antioxidant enzymes of plasma and brain tissue and total antioxidant capacity in plasma decreased significantly due to oxidative stress generated by MeHgCl. Administration in higher dose of both kind of linolenic acid restored all the activities of the antioxidant enzymes and also reduced lipid peroxidation and increased total antioxidant capacity in plasma. Both kinds of linolenic acid successfully maintained the RBC membrane integrity which was totally disrupted and became flat due to MeHgCl stress. α-Linolenic acid was more efficient antioxidant than α-eleostearic acid against oxidative DNA damage.     

Ameliorating effect of curcumin on sodium arsenite-induced oxidative damage and lipid peroxidation in different rat organs

The present study was conducted to investigate the antioxidative effect of curcumin against sodium arsenite-induced oxidative damage in rat. Animals were divided into four groups, the first group was used as control. Groups 2, 3 and 4 were orally treated with curcumin (15 mg/kg BW), sodium arsenite (Sa, 5 mg/kg BW) and sodium arsenite plus curcumin, respectively. Rats were orally administered their respective doses daily for 30 days. Results showed that Sa increased thiobarbituric acid-reactive substances (TBARS) in plasma, liver, kidney, lung, testes and brain. While, the activities of glutathione S-transferase, superoxide dismutase and catalase and the content of sulfhydryl groups (SH-groups) were significantly decreased in plasma and tissues compared to control. Treatment with curcumin alone reduced the levels of TBARS, while induced the activities of the antioxidant enzymes, and the levels of SH-groups. The presence of curcumin with Sa reduced the induction in the levels of TBARS and induced the decrease in the activities of antioxidant enzymes and the levels of SH-groups. Results indicated that treatment with Sa decreased body weight and increased liver weight compared to control. The presence of curcumin with Sa alleviated its toxic effects. It can be concluded that curcumin has beneficial influences and could be able to antagonize Sa toxicity.     

Studies on comparative efficacy of α-linolenic acid and α-eleostearic acid on prevention of organic mercury-induced oxidative stress in kidney and liver of rat

The present study was undertaken to evaluate the effect of α-linolenic acid and α-eleostearic acid, two isomers of linolenic acid, against oxidative stress induced by organic mercury in kidney and liver cells of rat. Male albino rats were divided into six groups. Groups 1, 2 were normal control and methyl mercury chloride (MeHgCl) treated (5 mg/kg BW/day) control, respectively. Groups 3, 4, 5 and 6 were orally treated with different doses of two fatty acids (0.5% and 1.0% of total lipid given for each isomer) along with MeHgCl (5 mg/kg BW). Results showed that activity of antioxidant enzymes viz. catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), reduced glutathione (GSH) in liver and kidney decreased significantly due to oxidative stress generated by MeHg. Administration of the linolenic acid isomers almost restored all the altered parameters and also reduced lipid peroxidation and leakage of trans-aminase enzymes from liver to blood due to liver injury when administrated in higher doses. Histopathology of liver and kidney cells showed that administration of α-linolenic acid significantly reduced the damage generated by MeHg. Thus, α-linolenic acid and α-eleostearic acid could serve as cost-effective and natural phytochemical preparation to protect against the adverse effects caused by organic mercury in human.     

Sodium arsenite induced biochemical perturbations in rats: ameliorating effect of curcumin

The present study was undertaken to evaluate the therapeutic efficacy of curcumin in terms of normalization of altered biochemical parameters following sodium arsenite treatment in rats. Animals were divided into four groups. The first group was used as control. While, groups 2, 3 and 4 were orally treated with curcumin (Cur, 15 mg/kg BW), sodium arsenite (Sa, 5 mg/kg BW) and sodium arsenite plus curcumin, respectively. Results showed that the activities of transaminases and phosphatases were significantly decreased in liver due to Sa administration, whereas increased in plasma. The activity of brain and plasma acetylcholinesterase (AChE) was decreased in rats treated with Sa. Also, Sa significantly decreased plasma total protein (TP), albumin (Alb) and high density lipoprotein-cholesterol (HDL-c), while increased glucose, urea, creatinine, bilirubin, total lipid (TL), cholesterol, triglyceride (TG) and low density lipoprotein-cholesterol (LDL-c). Curcumin alone decreased the levels of glucose, urea, creatinine, TL, cholesterol, TG and LDL-c. Curcumin reduced Sa-induced transaminases, phosphatases, glucose, urea, creatinine, bilirubin, TL, cholesterol and TG. Moreover, curcumin induced Sa-reduced liver transaminases and phosphatases, plasma and brain AChE, and the levels of TP and Alb. Experimental results, therefore suggested that curcumin protects arsenic induced biochemical alterations in rats.     

Alpha-lipoic acid protects oxidative stress,changes in cholinergic system and tissue histopathology during co-exposure to arsenic-dichlorvos in rats

We investigated protective efficacy of α-lipoic acid (LA), an antioxidant against arsenic and DDVP co-exposed rats. Biochemical variables suggestive of oxidative stress, neurological dysfunction, and tissue histopathological alterations were determined. Male rats were exposed either to 50 ppm sodium arsenite in drinking water or in combination with DDVP (4 mg/kg, subcutaneously) for 10 weeks. α-Lipoic acid (50 mg/kg, pos) was also co-administered in above groups. Arsenic exposure led to significant oxidative stress along, hepatotoxicity, hematotoxicity and altered brain biogenic amines levels accompanied by increased arsenic accumulation in blood and tissues. These altered biochemical variables were supported by histopathological examinations leading to oxidative stress and cell death. These biochemical alterations were significantly restored by co-administration of α-lipoic acid with arsenic and DDVP alone and concomitantly. The results indicate that arsenic and DDVP induced oxidative stress and cholinergic dysfunction can be significantly protected by the supplementation of α-lipoic acid.     

Sodium arsenite-induced cardiotoxicity in rats: protective role of p-coumaric acid,a common dietary polyphenol

Abstract

This study was performed to investigate the ameliorative role of p-coumaric acid against sodium arsenite-induced cardiotoxicity in rats. Sodium arsenite (5?mg/kg/b.wt) was orally administered once a day for 30 days to the animals to induce cardiotoxicity. After the experimental period, cardiotoxicity was assessed by estimating the levels of lipid peroxidation, anti-oxidant status (superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase, glutathione reductase, total reduced glutathione, protein sulfyhydryl and non-protein sulfhydryl groups) and DNA fragmentation in the cardiac tissue of control and experimental rats. In addition, cardiac tissue specific serum markers (triacylglycerides, total cholesterol, low-density lipoprotein cholesterol and high density lipoprotein cholesterol) in serum and histopathological changes in the cardiac tissue were also evaluated. From the results obtained in our study, sodium arsenite administration to the rats increased lipid peroxidation, DNA fragmentation, triacylglycerides, total cholesterol and low-density lipoprotein cholesterol, whereas antioxidant status and high-density lipoprotein cholesterol were found to be reduced. However, p-coumaric acid (75 and100?mg/kg/b.wt) treatment orally once per day for 30 days, immediately before a daily administration of sodium arsenite protected the abnormal biochemical abnormalities observed in the cardiac tissue of sodium arsenite treated rats as evidenced by the cardiac histopathology. For comparison purpose, a standard antioxidant vitamin C (100?mg/kg/b.wt) was used. In conclusion, this study concluded that p-coumaric acid could be a promising candidate for protecting the sodium arsenite-induced cardiotoxicity in rats through its antioxidant character.     

Effect of caffeic acid and rofecoxib and their combination against intrastriatal quinolinic acid induced oxidative damage, mitochondrial and histological alterations in rats

Oxidative stress has long been implicated in the neurotoxic effects of glutamate acting through N-methyl-D-aspartate (NMDA) receptors. Therefore, present study has been designed to explore the effect of rofecoxib and caffeic acid on the involvement of oxidative stress, mitochondrial dysfunction and neuronal linked with NMDA receptor-mediated excitotoxicity. Caffeic acid, is a well-known antioxidant flavanoid, implicate anti-inflammatory and immunomodulatory like actions. The present study is an attempt to investigate the antioxidant-like effect of caffeic acid and rofecoxib and their combination against QA-induced oxidative damage, mitochondrial dysfunction and histological alterations. Intrastriatal injection of quinolinic acid (300 nmol) significantly increased oxidative stress (raised lipid peroxidation, nitrite concentration, depleted SOD and catalase), altered mitochondrial complex enzyme activities and histological alteration in the ex vivo striatum. Caffeic acid (5 and 10 mg/kg, p.o.) and rofecoxib (10 and 20 mg/kg, p.o.) treatment for 21 days significantly attenuated oxidative damage and impairment in mitochondrial activities of complex enzymes in the ex vivo striatum. Further, combination of sub effective doses of rofecoxib (10 mg/kg, p.o.) and caffeic acid (5 mg/kg, p.o.) potentiated their protective effect which was significant as compared to their effect per se. The present study suggests the therapeutic effect of caffeic acid and rofecoxib combination against QA-induced ex vivo oxidative damage, mitochondrial and histological alterations in rats.     

Ability of Lactobacillus casei and Lactobacillus reuteri to protect against oxidative stress in rats fed aflatoxins-contaminated diet

Lactic acid bacteria (LAB) have been reported to remove mycotoxins from aqueous solutions through a binding process, which appears to be species and strain specific. The aim of the current study was to evaluate the protective role of Lactobacillus casei (L1) and Lactobacillus reuteri (L2) against aflatoxin (AFs)-induced oxidative stress in rats. Sixty female Sprague-Dawley rats were divided into 6 groups including the control group and the groups treated with L1 or L2 (1 × 10¹¹/ml) alone at a dose of 10 ml/kg b.w or plus AFs (3 mg/kg diet) for 4 weeks. At the end of the treatments, blood and tissue samples were collected for biochemical and histological studies. The results indicated that AFs alone induced a significant decrease in food intake and body weight and a significant increase in transaminase, alkaline phosphatase cholesterol, triglycerides, total lipids, creatinine, uric acid and nitric oxide in serum and lipid peroxidation in liver and kidney accompanied with a significant decrease in total antioxidant capacity. Treatments with L1 or L2 succeeded to induce a significant improvement in all the biochemical parameters and histological picture of the liver. Moreover, L2 was more effective than L1 and both can be used safely in functional foods.     

Reversal of propoxur-induced impairment of step-down passive avoidance, transfer latency and oxidative stress by piracetam and ascorbic acid in rats

Propoxur, a carbamate pesticide has been shown to adversely affect memory and induce oxidative stress. The present study was designed to correlate the effect of propoxur, piracetam (a nootropic drug) and ascorbic acid (an antioxidant) on oxidative stress and cognitive function. Cognitive function was assessed using step-down latency (SDL) on a passive avoidance apparatus and transfer latency (TL) on elevated plus maze. Oxidative stress was assessed by examining brain malondialdehyde (MDA) and non-protein thiol (NP-SH) levels. A significant reduction in SDL and prolongation of TL was found for the propoxur-treated group at weeks 6 and 7 as compared with control (p < 0.001). One week treatment by piracetam (400 mg/kg/d, i.p.) or ascorbic acid (120 mg/kg/d, i.p.) antagonized the effect of propoxur on SDL as well as TL. Both piracetam and ascorbic acid attenuated the propoxur-induced increase in brain MDA levels and decrease in brain NP-SH levels. Results of the present study show that ascorbic acid and piracetam have the potential to reverse cognitive dysfunction and oxidative stress induced by propoxur in the brain.     

Arsenic intoxication-induced reduction of glutathione level and of the activity of related enzymes in rat brain regions: reversal by dl-α-lipoic acid

The purpose of this study was to examine the effects of dl--lipoic acid (LA) on arsenic (As) induced alteration of glutathione (GSH) level and of the activity of glutathione-related enzymes—glutathione peroxidase (GSH-Px), glutathione reductase (GR), and glucose-6-phosphate dehydrogenase (G6PDH)—in rat brain regions (cortex, hypothalamus, striatum, cerebellum and hippocampus). Male Wistar rats of 150±10 g weight were divided into four groups: control and three experimental groups supplemented with arsenic (sodium arsenite) alone (100 ppm mixed in drinking water), lipoic acid alone (70 mg kg^–1 body weight), arsenic plus lipoic acid (100 ppm arsenic in drinking water plus 70 mg lipoic acid kg^–1 body weight). The arsenic content of brain regions was found to increase with the administration of sodium arsenite. Arsenic exposure elicited a significant decline in glutathione content and in the activity of related enzymes, with the greatest decreases seen in the cortex, striatum, and hippocampus, whereas there were no significant differences between control rats and the group treated with lipoic acid alone. Highly elevated content of the thiobarbituric acid-reactive substance malondialdehyde (MDA) in the brain regions of arsenic-exposed rats reflected extensive lipid peroxidation (LPO) processes. Simultaneous lipoic acid treatment was effective in reducing brain regional arsenic levels and lipid peroxidation and in increasing the glutathione content and the activity of its related enzymes. Lipoic acid, by acting as an alternative sulfhydryl nucleophile to glutathione, prevents its oxidation to glutathione disulfide in detoxifying reactions against reactive oxygen species and consequently increases the activity of glutathione-related enzymes.     

Protection of arsenic-induced hepatic disorder by arjunolic acid

Arsenic is one of the ubiquitous environmental pollutants, which affects nearly all organ systems. The present study has been carried out to investigate the hepatoprotective role of arjunolic acid, a triterpenoid saponin, against arsenic-induced oxidative damages in murine livers. Administration of sodium arsenite at a dose of 10 mg/kg body weight for 2 days significantly reduced the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione S-transferase, glutathione reductase and glutathione peroxidase as well as depleted the level of reduced glutathione and total thiols. In addition, sodium arsenite also increased the activities of serum marker enzymes, alanine transaminase and alkaline phosphatase, enhanced DNA fragmentation, protein carbonyl content, lipid peroxidation end-products and the level of oxidized glutathione. Studies with arjunolic acid show that in vitro it possesses free radical-scavenging and in vivo antioxidant activities. Treatment with arjunolic acid at a dose of 20 mg/kg body weight for 4 days prior to arsenic administration prevents the alterations of the activities of all antioxidant indices and levels of the other parameters studied. Histological studies revealed less centrilobular necrosis in the liver treated with arjunolic acid prior to arsenic intoxication compared to the liver treated with the toxin alone. Effects of a known antioxidant, vitamin C, have been included in the study as a positive control. In conclusion, the results suggest that arjunolic acid possesses the ability to attenuate arsenic-induced oxidative stress in murine liver probably via its antioxidant activity.     

Combination of chlorogenic acid and salvianolic acid B protects against polychlorinated biphenyls-induced oxidative stress through Nrf2

Caffeic acid derivatives (CADs) are well-known phytochemicals with multiple physiological and pharmacological activities. This study aimed to investigate the combined protective effects of CADs on PCB126-induced liver damages and oxidative stress in mice. Here, we used chemiluminescence and chose chlorogenic acid (CGA), salvianolic acid B (Sal B) as the best antioxidants. Then, mice were intragastrically administered with 60 mg/kg/d CGA, Sal B, and CGA plus Sal B (1:1) for 3 weeks before exposing to 0.05 mg/kg/d PCB126 for 2 weeks. We found that pretreatment with CGA, Sal B, and CGA plus Sal B effectively attenuated liver injury and cytotoxicity caused by PCB126, but improved the expressions of superoxide dismutase (SOD), glutathione reduced (GSH), heme oxygenase-1 (HO-1) and nuclear factor E2-related factor 2 (Nrf2), CGA plus Sal B especially, was found to have the best effects that indicated a synergetic protective effect. Taken together, as the Nrf2 regulates the cyto-protective response by up-regulating the expression of antioxidant genes, we suggested that CGA plus Sal B had a combined protection on PCB126-induced tissue damages and that the Nrf2 signaling might be involved.     

Synergistic effect of the combination of gallic acid and famotidine in protection of rat gastric mucosa

BackgroundAntioxidant supplements with existing drugs may confer better therapeutic efficacy in oxidative stress related diseases. The purpose of the present work was to characterize the interaction and investigate the protective effect of H₂ blocker famotidine and gallic acid in combination against experimentally induced peptic ulcer.MethodsPreventive effect of gallic acid and famotidine in different combinations was investigated against aspirin plus pyloric ligation induced ulcer in rat. Ulcer index, gastric juice volume, pH, other biochemical parameters of gastric juice and antioxidant activity using stomach tissue were estimated.ResultsPretreatment with gallic acid and famotidine in combinations for 7 days, protected the gastric mucosa significantly (p < 0.05, 0.01), which was evidenced by decrease in ulcer index, gastric juice volume, free and total acidity, total protein, pepsin and DNA content, and increase in pH, carbohydrates concentration in gastric juice. Combination treatment increases levels of superoxide dismutase, catalase, reduced glutathione, glutathione reductase and glucose-6-phosphate dehydrogenase, and decreases lipid peroxidation, myloperoxidase in stomach tissue. Along with higher dose combination, lower dose combinations like gallic acid (50 mg/kg) plus famotidine (10 mg/kg) also offered better antiulcer activity than their individual effect. Histopathological studies confirmed their antiulcer activity.ConclusionCombination treatments confer synergistic protective effect against peptic ulcer in rats, which was related to the gastroprotective, antisecratory and antioxidant activity of combination treatment. Results proved that use of gallic acid with existing antiulcer drug will be more useful in the prevention/management of peptic ulcer.     

Systematic evaluation of the antioxidant potential of different parts of Foeniculum vulgare Mill. from Portugal

Fennel (Foeniculum vulgare Mill.) is a widespread perennial umbeliferous (Apiaceae) herb, traditionally used for medicinal purposes and human consumption. It is highly recommended for diabetes, bronchitis and chronic coughs, and for the treatment of kidney stones; some of those chronic diseases are related to the production of radical species involved in the oxidative stress. Therefore, the antioxidant potential of this herb might explain some of their empirical uses in folk medicine. This is the first time that a systematic study on different parts of fennel is performed, in order to understand differences in the antioxidant potential of shoots, leaves, steams, and inflorescences, particularly related to their composition in antioxidant compounds such as vitamins (ascorbic acid and tocopherols) and phenolics. The shoots seems to have the highest radical-scavenging activity and lipid peroxidation inhibition capacity (EC₅₀ values < 1.4 mg/ml), which is in agreement with the highest content in phenolics (65.85 ± 0.74 mg/g) and ascorbic acid (570.89 ± 0.01 μg/g) found in this part. The shoots also revealed high concentration of tocopherols (34.54 ± 1.28 μg/g) and were the only part with flavonoids.     

Alteration of lipid status and lipid metabolism,induction of oxidative stress and lipid peroxidation by 2,4-dichlorophenoxyacetic herbicide in rat liver

Abstract

This study aims to investigate the effects of the 2,4-dichlorophenoxyacetic herbicide (2,4-D) on plasma lipids, lipoproteins concentrations, hepatic lipid peroxidation, fatty acid composition and antioxidant enzyme activities in rats. Animals were randomly divided into four groups of 10 each: control group and three 2,4-D-treated groups G1, G2 and G3 were administered 15, 75 and 150?mg/kg/BW/d 2,4-D by gavage for 28?d, respectively. Results showed that 2,4-D caused significant negative changes in the biochemical parameters investigated. The malondialdehyde level was significantly increased in 2,4-D-treated groups. Fatty acid composition of the liver was also significantly changed with 2,4-D exposure. Furthermore, the hepatic antioxidant enzyme activities were significantly affected. Finally, 2,4-D at the studied doses modifies lipidic status, disrupt lipid metabolism and induce hepatic oxidative stress. In conclusion, at higher doses, 2,4-D may play an important role in the development of vascular disease via metabolic disorder of lipoproteins, lipid peroxidation and oxidative stress.     

Effects of lipoic acid and n-3 long-chain polyunsaturated fatty acid on the liver ovariectomized rat model of menopause

Background

Bilateral ovariectomy is an experimental model used to analyse the effects of menopause and develop strategies to mitigate the deleterious effects of this condition. Supplementation of the diet with antioxidants has been used to reduce potential oxidative stress caused by menopause. The purpose of the study was to analyse the effects of α-lipoic acid (LA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), dietary supplementation on oxidative stress in the livers of ovariectomized rats.

Food preservative sorbic acid deregulates hepatic fatty acid metabolism

Sorbic acid (SA) is one of the most commonly used food preservatives worldwide. Despite SA having no hepatotoxicity at legal dosages, its effect on hepatic lipid metabolism is still unclear. We investigated the effect of SA on hepatic lipid metabolism and its mechanism of action in C57BL/6 mice. Daily treatment with SA (1 g/kg in diet) for 4 weeks did not alter the body weight, organ weight, and blood lipids in mice. However, hepatic lipid accumulation, particularly that of triglycerides, fatty acids, and glycerol, but not cholesteryl ester and free cholesterol, was increased with SA treatment. Mechanistically, SA decreased the expression of proteins related to de novo fatty acid lipogenesis, fatty acid internalization, and very low-density lipoprotein (VLDL) secretion-related pathways, including sterol regulatory element-binding proteins, acetyl-coA carboxylase, fatty acid synthase, liver fatty acid-binding protein, CD36, and apolipoprotein E. In contrast, SA increased the expression of diacylglycerol O-acyltransferase 2, the key enzyme for triacylglycerol synthesis. Moreover, SA downregulated the protein expression of autophagy-related and β-oxidation-related pathways, the two major metabolic pathways for lipid metabolism, including LC-3, beclin-1, autophagy related protein 5 (ATG-5) and ATG-7, acyl-CoA synthetase long chain family member 1, carnitine palmitoyltransferase Iα, peroxisome proliferator-activated receptor α (PPARα), PPARγ, and PPARγ coactivator-1. Collectively, SA deregulates de novo lipogenesis and fatty acid internalization, VLDL secretion, autophagy, and β-oxidation in the liver, leading to impaired lipid clearance and ultimately, resulting in lipid accumulation in the liver.     

The ameliorating effects of selenium and vitamin C against fenitrothion-induced blood toxicity in Wistar rats

Fenitrothion is widely used organophosphate pesticide in agriculture and health programs, but besides, it causes several toxic effects. The present study was designed to evaluate the possible protective effects of selenium (0.5 mg/kg b.w.) and vitamin C (100 mg/kg b.w) on altered haematological, biochemical and oxidative stress parameters in the blood of rats orally treated with fenitrothion (20 mg/kg b.w) for 30 days. Fenitrothion caused changes in body weight, food and water intake, and some haematological and biochemical parameters. Fenitrothion altered the glutathione redox status (GSH and GSSG) and decreased activity of antioxidant enzymes (GSH-Px, GST, SOD and CAT), leading to a lipid peroxidation. Selenium and vitamin C, by improving the activity of antioxidants, reduced oxidative stress and a lipid peroxidation, maintaining the values of examined parameters to optimal levels. Therefore, selenium and vitamin C could be useful in providing protection of exposed non-target organisms including people from fenitrothion.     

Perfluorononanoic acid induces apoptosis involving the Fas death receptor signaling pathway in rat testis

Perfluorononanoic acid (PFNA, C9), a synthetic perfluorinated chemical containing nine carbons, accumulates and is biomagnified through food webs. This compound has been detected in the serum of humans and wildlife and has the potential for reproductive interference. Few studies, however, have reported the effects of PFNA exposure on male reproduction. To determine this, male rats were orally dosed for 1, 3 and 5 mg/kg day PFNA or with vehicle for 14 days. In the present study, serum testosterone levels were decreased, while estradiol levels were increased dramatically in rats receiving 5 mg PFNA/kg day. Spermatogenic cells from rats that received 5 mg PFNA/kg day exhibited apoptotic features including crescent chromatin condensation and chromatin margination. Flow cytometric analysis and TUNEL assays revealed a dose-dependent increase of apoptotic cell numbers. In addition, expression of Fas and Bax mRNA levels were upregulated significantly, and Bcl-2 mRNA levels were downregulated markedly in the 3 and 5 mg/kg day groups. A dose-dependent increase in levels of active caspase-8 and no significant changes of active caspase-9 were observed. Our results indicate that PFNA exposure can lead to cell apoptosis in rat testis, and this apoptosis was probably associated with the Fas death receptor-dependent apoptotic pathway.