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The aim of this study was to analyze the biochemical alterations in the gills of Venus verrucosa under exposure for 6 days to three doses of lambda-cyhalothrin (λ-cyh) (100, 250, and 500 µg L -1 ). Malondialdehyde, lipid hydroperoxide, and hydrogen peroxide levels in the gills of treated groups increased. λ-Cyh exposure significantly increased the protein carbonyl and reduced glutathione levels in the gills of all treated groups. Moreover, the activities of superoxide dismutase and glutathione peroxidase were increased. In our study, the polyunsaturated fatty acid (FA), omega-6, eicosapentaenoic acid (C20:5n-3), and docosahexaenoic acid (C22:6n-3) were increased in the treated groups. A significant decrease in the saturated FAs, omega-3, and arachidonic acid (C20:4n-6) levels was observed. The content of monounsaturated FA was changed in the groups treated with 100 and 250 µg L -1 of λ-cyh. As a corollary, desaturase and elongase activities were significantly increased. Our study provides evidence of the underlying toxic mechanism of λ-cyh and its capacity to create oxidative stress and revealed that FA profiling is a new approach for elucidating the λ-cyh toxicity.

Hexavalent chromium (chromium (VI)), a highly toxic heavy metal, is a common pollutant of aquatic ecosystems. The present study aimed to elucidate the potential toxic effects of chromium (VI) on oxidative stress biomarkers and fatty acids profile in the gills and digestive gland of Venus verrucosa, an ecologically and economically important bivalve species. Three doses of chromium (VI) (1, 10 and 100 μg.L -1 ) were chosen for V. verrucosa exposure during 7 days under controlled conditions. A significant increase in the levels of malondialdehyde, lipid hydroperoxides and hydrogen peroxide was observed in the gills and digestive gland of chromium (VI)-exposed V. verrucosa as compared to the control group. Furthermore, an induction of enzymatic antioxidant activities (superoxide dismutase, glutathione peroxidase and glutathione S-transferase) and an enhancement of non-enzymatic antioxidant levels (non-protein thiols, glutathione and vitamin C) were marked. An alteration of fatty acids composition was also noted following chromium (VI) exposure. The obtained results highlighted the importance of assessing oxidative damage biomarkers and fatty acids profile in the study of chromium (VI)-induced toxicity in V. verrucosa., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Mercury is one of the most harmful pollutant that threat marine biota. This study assessed the Hg impact on the fatty acid (FA) composition and the antioxidant statues in Holothuria forskali body wall tissue. Specimens were exposed to HgCl 2 graded doses (40, 80 and 160 μg L -1 ) for 96 h. A decrease in linoleic, arachidonic and eicosapentaenoic acid levels and an increase of docosahexaenoic acid were mainly observed at the nominal tested dose. The exposure to the upper dose promoted oxidative stress with an increase of malondialdehyde, hydrogen peroxide, advanced oxidation protein product, glutathione and non-protein thiols levels. Moreover, a decrease in catalase and an increase in superoxide dismutase and glutathione peroxidase activities were observed. Yet, an increase of the metallothionein level was registered in all treated groups. This study confirmed the Hg toxicity on the redox statue of H. forskali and highlighted the usefulness of the FA composition as an early sensitive bioindicators., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The present study was performed to evaluate the protective effect of selenium (Se) against penconazole (PEN)-induced oxidative stress in the cardiac tissue of adult rats. Male Wistar rats were divided into four groups of six each. The first group represented the controls. For the second group (PEN), no treatment was performed during the first 6 days, and then, the rats received intraperitoneally 67 mg/kg body weight (bw) of PEN every 2 days from day 7 until day 15, the sacrifice day. For the third group (Se + PEN), Se was administered daily through the diet at a dose of 0.5 mg/kg of diet for 15 days. Rats of this group received also every 2 days PEN (67 mg/kg bw) from day 7 until day 15. The fourth group (Se) received daily, through the diet, Se (0.5 mg/Kg of diet) during 15 days. Our results showed that Se reduced significantly the elevated cardiac levels of malondialdehyde and protein carbonyl following PEN treatment, and attenuated DNA fragmentation induced by this fungicide. In addition, Se modulated the alterations of antioxidant status: enzymatic (superoxide dismutase, glutathione peroxidase, and catalase) and nonenzymatic (glutathione and vitamin C) antioxidants in the heart of PEN-treated rats. This trace element was also able to alleviate perturbations of lipid profile. The protective effect of selenium was further evident through the histopathological changes produced by PEN in the heart tissue. Taken together, our results indicated that Se might be beneficial against PEN-induced cardiac oxidative damage in rats.

Fenthion (FEN) is an organophosphorus pesticide known for its wide toxic manifestations. In this study, the effects of FEN were evaluated on the cerebrum and cerebellum oxidant/antioxidant status and histopathological disorders in the suckling rats. Pregnant rats were divided into two groups: control group received pure water, while FEN group received daily by their drinking water 551 ppm of FEN from the 14th day of pregnancy until day 14 after delivery. Acetylcholine esterase (AChE) activity was inhibited in both the cerebrum and cerebellum of suckling rats whose mothers were treated with FEN. The cerebrum and cerebellum oxidative damage was demonstrated by a significant increase of malondialdehyde (MDA), advanced oxidation protein product and glutathione (GSH) levels and disturbance in the antioxidant enzyme activities. A significant decline of non-protein thiol and vitamin C levels was also observed. These changes were confirmed by histopathological observations which were marked by pyknotic neurons in the cerebrum and apoptotic cells in the cerebellum of FEN-treated rats. In the cerebellum of FEN-treated rats, the most conspicuous damage was the absence of external granular layer, indicating growth retardation. These data suggested that exposure of pregnant and lactating rats to FEN induced oxidative stress and histopathological disorders in the cerebrum and cerebellum of their pups. Thus, the use of FEN must be under strict control, especially for pregnant and lactating mothers.

Dimethoate (DM) is an organophosphate insecticide widely used in agriculture and industry and has toxic effects on non-target organisms especially mammalian. However, we still know little about DM-induced kidney injury and its alleviation by natural antioxidants. In the present study, selenium (Se), vitamin E, DM, Se+DM, vitamin E+DM, Se+vitamin E+DM were given to adult rats for 4 weeks. Plasma creatinine and uric acid, kidney MDA, PC, H2O2 and AOPP levels were higher, while Na(+)-K(+)-ATPase and LDH values were lower in the DM group than those of controls. A smear without ladder formation on agarose gel was shown in the DM group, indicating random DNA degradation and DM-induced genotoxicity. A decrease in kidney GSH, NPSH and plasma urea levels and an increase in GPx, SOD and catalase activities were observed in the DM group when compared to those of controls. Plasma cystatin C levels increased, indicating a decrease in glomerular filtration rate. When Se or vitamin E was added through diet, the biochemical parameters cited above were partially restored in Se+DM and vitamin E+DM than DM group. The joint effect of Se and vitamin E was more powerful against DM-induced oxidative stress and kidney dysfunction. The changes in biochemical parameters were substantiated by histological data. In conclusion, our results indicated a possible mechanism of DM-induced nephrotoxicity, where renal genotoxicity was noted, membrane-bound ATPases and plasma biomarkers were disturbed. Se and vitamin E ameliorated the toxic effects of this pesticide in renal tissue suggesting their role as potential antioxidants.

There is considerable interest in the study of free radical-mediated damage to biological systems due to pesticide exposure. However, there is a lack of consensus as to which determinations are best used to quantify future risks arising from xenobiotic exposure and natural antioxidant interventions. Our study investigated the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate cardiotoxicity induced by dimethoate. Female Wistar rats were exposed for 30 days either to dimethoate (0.2 g L⁻¹ of drinking water), dimethoate+selenium (0.5 mg kg⁻¹ of diet), dimethoate+vitamin E (100 mg kg⁻¹ of diet), or dimethoate+selenium+vitamin E. The exposure of rats to dimethoate promoted oxidative stress with a rise in malondialdehyde, advanced protein oxidation, and protein carbonyl levels. An increase of glutathione peroxidase, superoxide dismutase, and catalase activities was also noted. A fall in acetylcholinesterase and Na⁺ K⁺-ATPase activities, glutathione, nonprotein thiols, vitamins C and E levels was observed. Plasma levels of cholesterol, triglycerides, and low density lipoprotein-cholesterol increased and those of high density lipoprotein-cholesterol decreased. Coadministration of selenium or vitamin E to the diet of dimethoate-treated rats ameliorated the biochemical parameters cited above. The histopathological findings confirmed the biochemical results and the potential protective effects of selenium and vitamin E against cardiotoxicity induced by dimethoate., (Copyright © 2011 Wiley Periodicals, Inc., A Wiley Company.)

The aim of this study was to evaluate the biochemical changes in cobalt-exposed rats and to investigate the potential role of Tunisian propolis against the cobalt-induced renal damages. Twenty-four pregnant Wistar rats were divided into four groups and were treated as follows: group 1 (control) received distilled water; group 2 received 350 ppm of CoCl(2) in drinking water; group 3 received 350 ppm CoCl(2) in drinking water and a propolis-supplemented diet (1 g/100 g of diet); group 4 received a propolis-supplemented diet (1 g/100 g of diet) without cobalt. In the cobalt group, a significant decrease in body, absolute and relative weights was noted when compared to controls. The administration of cobalt to pregnant rats from the 14th day of pregnancy until day 14 after delivery resulted in an increased level of renal malondialdehyde, a decreased renal content of glutathione and antioxidant enzyme activities such as superoxide dismutase, catalase and glutathione peroxidase in lactating rats and their pups. A statistically significant increase in plasma urea and creatinine serum levels was seen in treated female rats and their pups. Histopathologically, the cobalt-administration induced degenerative changes in the kidney of lactating rats and their pups. When compared with cobalt-treated rats, those receiving the propolis supplementation (along with cobalt-treatment) had lower malondialdehyde levels, higher antioxidant activities and the cobalt-related histopathological changes in the kidneys were at lower severity. Our results suggested that the propolis might be a potential candidate agent against cobalt-induced nephrotoxicity in adult and juvenile rats when administered to female rats during the late pregnancy and the early postnatal period., (Copyright © 2011 Elsevier GmbH. All rights reserved.)

Chromium is known for its wide toxic manifestations. This experiment aims to evaluate the effect of selenium against oxidative stress induced by chromium in the cerebrum and cerebellum. Female Wistar rats were randomly divided into four groups of six each: group I served as controls which received the standard diet; group II received drinking water K(2)Cr(2)O(7) alone (700 ppm); group III received both K(2)Cr(2)O(7) and Se (0.5 mg Na(2)SeO(3)/kg of diet); and group IV received Se (0.5 mg/kg of diet) for 3 weeks. The exposure of rats to K(2)Cr(2)O(7) promoted oxidative stress in the cerebrum and cerebellum with an increase in malondialdehyde and a decrease of nonenzymatic antioxidant levels such as glutathione, nonprotein thiol, and vitamin C. An increase of enzyme activities like catalase, glutathione peroxidase, and superoxide dismutase activities was also observed. Acetylcholinesterase activity was inhibited after treatment with K(2)Cr(2)O(7). Co-administration of Se restored the parameters cited above. The histopathological findings confirmed the biochemical results.

Chronic hyperglycemia in diabetes leads to free radicals overproduction, which contributes to the development of diabetic nephropathy. The present study investigated the effects of Artemisia campestris (Ac), a plant of the Asteraceae family, on renal impairment and oxidative stress in alloxan-induced diabetic rats. Diabetes was induced by a single subcutaneous injection of alloxan (120 mg kg(-1)) in rats. Ac (200 mg kg(-1)) was administered to diabetic rats for 3 weeks. Diabetic renal injury was associated with hyperglycemia, increased serum creatinine, urea and uric acid levels. This nephropathophysiology was associated with a surproduction of nitric oxide (NO), malondialdehyde (MDA) and advanced oxidation protein products (AOPP) levels and a decrease in glutathione (GSH) levels. In addition, hyperglycemia increased the activities of antioxidant enzymes, such as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx), in the kidney of diabetic rats. Treatment with Ac effectively ameliorated diabetic renal dysfunction by reducing oxidative and nitrosative stress. Histological studies also supported the experimental findings. The results suggested that Ac might act as a beneficial agent against renal dysfunctions developed in alloxan-induced diabetes., (Copyright © 2012 Elsevier GmbH. All rights reserved.)

Aims: Selenium has a pharmacological properties and it is well considered as an antioxidant. The present study investigated the potential ability of selenium, used as a nutritional supplement, to alleviate bone impairments in suckling rats whose mothers were treated with methimazole, an antithyroid drug., Main Methods: Female Wistar rats were randomly divided into four groups of six each: group I served as control which received standard diet; group II were rendered hypothyroid by administration of methimazole (250 mg L(-1) in their drinking water); group III received both methimazole (250 mg L(-1) in their drinking water) and selenium (0.5 mg kg(-1) of diet); group IV received 0.5 Na(2)SeO(3) mg kg(-1) of diet. Treatments were started from the 14th day of pregnancy until day 14 after delivery., Key Findings: Methimazole treatment decreased femur length and weight in 14-day-old rats, when compared to controls. Femur antioxidant enzyme activities, superoxide dismutase, catalase and glutathione peroxidase decreased. Lipid peroxidation recorded an increase revealed by high femur malondialdehyde levels. Methimazole also caused a significant decrease in calcium and phosphorus levels in bone. Yet, in plasma and urine, they increased and decreased inversely. Besides, plasma total tartrate-resistant acid phosphatase was enhanced, while total alkaline phosphatase was reduced. Co-administration of selenium through diet improved the biochemical parameters cited above. Nevertheless, distorted histoarchitecture revealed in hypothyroid rat femur was alleviated by Se treatment., Significance: The present study suggests that selenium is an important protective element that may be used as a dietary supplement protecting against bone impairments., (Copyright © 2010 Elsevier GmbH. All rights reserved.)

Chromium, a major environmental pollutant, is known for its wide toxic manifestations. The present experiment pertains to the protective role of selenium (Se) against K(2)Cr(2)O(7)-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 K(2)Cr(2)O(7) alone (700 ppm); group III received both K(2)Cr(2)O(7) and Se (0.5 Na(2)SeO(3) 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 K(2)Cr(2)O(7)-induced hepatotoxicity., (Copyright © 2010 Elsevier GmbH. All rights reserved.)

Acute exposure to pesticides can cause hepatotoxicity. Our study pertains to the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress induced by dimethoate. Female Wistar rats were randomly divided into seven groups of six each: group I served as controls; group II received in their drinking water dimethoate (2 g L(-1)); group III received both dimethoate and selenium (0.5 mg/kg of diet); group IV was treated with dimethoate and vitamin E (100 mg/kg of diet); group V received dimethoate+selenium+vitamin E and groups VI and VII received either selenium or vitamin E. The exposure of rats to dimethoate for 30 days promoted oxidative stress with an increase in malondialdehyde and a decrease in glutathione and non-protein thiol levels. A decrease in glutathione peroxidase, superoxide dismutase and catalase activities was also observed. While, plasma transaminases, lactate dehydrogenase activities and bilirubin levels increased. Co-administration of selenium and/or vitamin E through diet improved the biochemical parameters cited above. Liver histological studies confirmed biochemical parameters and the beneficial roles of selenium and vitamin E., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Context:Nitraria retusa(Forssk.) Asch. (Nitrariaceae) is a medicinal plant which produces edible fruits whose antioxidant activity has been demonstrated. Objective:The current study elucidates the potential protective effect ofN. retusafruit aqueous extract against nephrotoxicity induced by penconazole, a triazole fungicide, in the kidney of adult rats. Materials and methods:Adult Wistar rats were exposed either to penconazole (67 mg/kg body weight), or toN. retusaextract (300 mg/kg body weight) or to their combination. Penconazole was administered by intra-peritoneal injection every 2 days from day 7 until day 15, the sacrifice day, whileN. retusaextract was administered daily by gavage during 15 days. Oxidative stress parameters, kidney biomarkers and histopathological examination were determined. Results:Nitraria retusaextract administration to penconazole treated rats decreased kidney levels of malondialdehyde (−10%), hydrogen peroxide (−12%), protein carbonyls (PCOs, −11%) and advanced oxidation protein products (AOPP, −16%); antioxidant enzyme activities: catalase (−13%), superoxide dismutase (−8%) and glutathione peroxidase (GPx, −14%), and the levels of non-enzymatic antioxidants: non-protein thiols (−9%), glutathione (−7%) and metallothionein (−12%). Furthermore, this plant extract prevented kidney biomarker changes by reducing plasma levels of creatinine, urea, uric acid and LDH and increasing those of ALP and GGT. Histopathological alterations induced by penconazole (glomeruli fragmentation, Bowman’s space enlargement, tubular epithelial cells necrosis and infiltration of inflammatory leucocytes) were attenuated followingN. retusaadministration. Discussion and conclusion:Our results indicated thatN. retusafruit extract had protective effects against penconazole-induced kidney injury, which could be attributed to its phenolic compounds. [ABSTRACT FROM PUBLISHER]

Gibberellic acid (GA3) is a plant growth regulator used in agriculture worldwide. The present study investigated the propensity of GA3 to induce hematological disorders. Pregnant Wistar rats were randomly divided into two groups: group I served as controls; group II received orally GA3 (200 ppm) from the 14th day of pregnancy until day 14 after delivery. GA3 reduced the number of red blood cells, hemoglobin concentration, and hematocrit in suckling rats, while these parameters remained unchanged in their mothers. White blood cells increased in mothers and were unchanged in their pups. Several studies have associated these hematological disorders with oxidative stress. In fact, GA3 treatment revealed in erythrocytes a significant increase in malondialdehyde levels and a decrease in antioxidant enzyme activities such as superoxide dismutase, catalase, and glutathione peroxidase. Moreover, a significant decline was observed in acetylcholinesterase activity, glutathione, nonprotein thiols, and vitamin C levels. [ABSTRACT FROM AUTHOR]

Abstract: Pesticides have been used in agriculture to enhance food production by eradicating unwanted insects and controlling disease vectors, nevertheless occupational exposure to high levels of these compounds can lead to neurodegenerative disorders, characterized by serious oxidative and neurotoxic effects. However, there is a lack of consensus as to which determinations are best used to quantify future risks arising from xenobiotic exposure and natural antioxidant interventions. Our study aims to determine the potential ability of selenium and/or vitamin E, used as nutritional supplements, to alleviate oxidative stress in cerebral cortex tissue induced by dimethoate, an organophosphorus pesticide. Adult Wistar rats were exposed either to dimethoate (0.2g/L of drinking water), dimethoate+selenium (0.5mg/kg of diet), dimethoate+vitamin E (100mg/kg of diet), or dimethoate+selenium+vitamin E, for 30days. Exposure to dimethoate increased malondialdehyde levels, protein carbonyl groups and advanced oxidation protein products, while Na+K+-ATPase, acetylcholinesterase and butyrylcholinesterase activities decreased in the cerebral cortex. An increase in glutathione peroxidase, superoxide dismutase and catalase activities and a decrease in glutathione, non-protein thiols and vitamin C levels were observed. Administration of selenium and/or vitamin E through the diet in dimethoate treated rats ameliorated the biochemical parameters cited above. The histological findings confirmed the biochemical results. The model of this study that we employed characterized the relationships between dimethoate-induced neurotoxicity and its alleviation by natural antioxidants like selenium and vitamin E. These elements may be considered beneficial for the protection of cerebral cortex against injury induced by dimethoate. [Copyright &y& Elsevier]

Abstract: Fenthion (FEN) is an organophosphate insecticide used in both agricultural and urban areas throughout the world including Tunisia. Recent investigations have proved the crucial role of natural antioxidants to prevent the damage caused by toxic compounds. In this study, we investigated the role of Artemisia campestris (Ac) leaf powder in protection against oxidative damage and hepatotoxicity induced by fenthion in female rats and their pups. Female Wistar rats were divided into four groups: group I served as controls which received standard diet, group II received orally FEN 551ppm, group III received both 551ppm of FEN and experimental diet (5% Artemisia) and group IV received experimental diet (5% Artemisia). Oral administration 551ppm of FEN by drinking water to adult rats caused hepatotoxicity as monitored by the increase in the levels of hepatic markers enzymes (transaminases and lactate dehydrogenase), total cholesterol (TC) and triglycerides (TG), as well as hepatic malondialdehyde (MDA) levels thus causing a drastic alteration in antioxidant defence system. Particularly, the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) and the level of reduced glutathione (GSH) increased by FEN. These biochemical alterations were accompanied by histological changes marked by leucocytes infiltration, sinusoidal dilatation (moderate peliosis), granuloma inflammatory disorders and necrosis in hepatocytes of dams. While, slight leucocytes infiltration was shown in pups. Treatment with Ac prevented the liver damage induced by FEN, as revealed by inhibition of hepatic lipid peroxidation accompanied by an improvement of liver histopathological changes, CAT and GPx activities except GSH and SOD which were not modified. It could be concluded that A. campestris is promising a protective agent against hepatotoxicity during the exposure to fenthion. [Copyright &y& Elsevier]