Résumé: 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 coadministration 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. Mahfoud Messarah,Fahima Klibet, Amel Boumendjel, Cherif Abdennour, Noureddine Bouzerna, Mohamed Salah Boulakoud, Abdelfattah El Feki

Résumé: The aim of this study was to determine whether the effects of thyroid dysfunction induce oxidative stress in the blood and heart of male Wistar rats. Rats were randomly divided into three groups: group I served as control rats. Group II was treated daily with 0.05% benzythiouracile (BTU) administered in drinking water. Rats of group III have received l-thyroxine sodium salt (0.0012%), in drinking water. The results showed that thyroid dysfunction rats had poor growth performance. On the other hand, in hyperthyroid rats, a marked decrease compared with control occurred of some hematological parameters such red blood cell number (RBC), haemoglobin (Hb) concentration and haematocrit (Ht). There was also a significant increase in erythrocyte numbers and heart TBARS concentrations in hypothyroid rats compared with control. These results were associated with a fall in the total antioxidant status (TAS) in the serum of the hyperthyroid rats. Alteration of the antioxidant system in the hypo-/hyperthyroidism-induced rats was confirmed by the significant increase of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities and a decline in glutathione (GSH) content in both tissueswere detected in hyperthyroid group compared to controls. On the other hand, serum transaminase activities (aspartate transaminase (AST); alanine transaminase (ALT)) were elevated indicating hepatic cellular damage after treatment with exogenous l-thyroxine. Moreover, serum lactate dehydrogenase (LDH), gamma-glutamyl transferase (GGT) and creatine phosphokinase (CPK) activities were increased in the hyperthyroidism rats. These results indicated that excessive thyroxin (long term) ingestion had an adverse effect on animal health and performance.We conclude that thyroid dysfunction induces oxidative stress and modifies some biochemical parameters of erythrocytes, heart and liver disease; our results show the occurrence of a state of oxidizing stress in relation to hyperthyroidism. Mahfoud Messaraha,Mongi Saoudi, Amel Boumendjel, Mohamed Salah Boulakoud, Abdelfattah El Feki

Résumé: The purpose of this study was to evaluate the effects of dysthyroidism on lipid peroxidation,antioxidants status,liver, and serum dysfunction parameters in the hypo-/hyperthyroidism-induced rats.Hypothyroidism and hyperthyroidism conditions were induced for 5weeks by administration of0.05% benzythiouracile(BTU)and L-thyroxine sodium salt(0.0012%),in drinking water,respectively.The enzymatic activities of glutathione peroxidase (GPx),superoxide dismutase(SOD),catalase(CAT)and the lipid peroxidation product;thiobarbituric acid reacting substances(TBARS)were measured in liver as indicators of oxidative damage.However,liver dysfunction parameters represented by the activities of aspartate transaminase(AST),alanine transaminase(ALT),alkaline phosphatase (ALP),lactate dehydrogenase(LDH),and gammaglutamyltransferase(GGT),were measured in serum.In hyperthyroidism rats,the TBARS contents of liver have significantly increased compared to those in hypothyroid rats and the controls (po0.001),associated with a fall of the total antioxidant status(TAS)in the serum of the hyperthyroidrats.The SOD,CAT,and GPx activities in liver of hyperthyroid rats have significantly increased compared to hypothyroid rats and the controls(po0.001).The AST,ALT,LDH,GGT,and ALP activities increased in the hyperthyroidism rats(po0.05). We conclude that thyroid dysfunction induces oxidative stress and modifies some biochemical parameters of liver.Our results show the occurrence of a state of oxidizing stress in relation to hyperthyroidism. Messarah M, Boumendjel A., Chouabia A., Klibet F., Abdennour C., Boulakoud M.S., El Feki A.

Résumé: The effect of the thyroid activity on the formation of lipid peroxidation and on liver and heart antioxidant enzyme activities was investigated in Wistar rats. Hypothyroidism and hyperthyroidism conditions were induced for five weeks by the administration of 0.05% benzythiouracile (BTU) and L-thyroxine sodium salt (0.0012%), in drinking water, respectively. No significant effect was observed on the rates of both lipid peroxidation and the vitamin E in hepatic and cardiac tissues of hypothyroidism ratscompared to the controls, contrary to the hyperthyroidism rats, which expressed a pronounced increase. The increased glutathione peroxydase activity in rats suffering from hyperthyroidism was associated with a fall of the reduced glutathione in the homogenate and a marked increase in the glutathione reductase activity. An increase in superoxyde dismutase and catalase activities was also recorded in hyperthyroidism. Our results explain the thyroid activity variation in relation to the lipid peroxidation and the tissular contents of the enzymatic and the non-enzymatic antioxidants. To conclude, our results show the occurrence of a state of oxidizing stress in relation to hyperthyroidism. Messarah M, Boulakoud M.S., Boumendjel A., Abdennour C., El Feki A.