Nigella sativa oil reduces aluminium chloride-induced oxidative injury in liver and erythrocytes of rats.

The present study was planned to investigate the protective effects of Nigella sativa oil (NSO) supplementation against aluminium chloride (AlCl3)-induced oxidative damage in liver and erythrocytes of rats. Simultaneously, a preliminary phytochemical study was affected in order to characterize the bioactive components containing in the NSO using chemical assays. The antioxidant capacities of NSO were evaluated by DPPH assay. The results showed that NSO was found to contain large amounts of total phenolics, flavonoids and tannins. Twenty-four rats were equally divided into two groups, in which group A received standard diet, whereas group B treated daily with an oral gavage dose of 2 ml NSO/kg body weight. After 5 weeks pretreatment, both groups were divided again into two subgroups (A and B) of six animals each and treated for other 3 weeks. Therefore, subgroup A1 was served as a control which received standard diet, but subgroup A2 received AlCl3 (34 mg/kg bw mixed with food). Subgroup B1 received both AlCl3 and NSO; however, subgroup B2 received NSO only. Results showed that AlCl3 exhibited an increase in white blood cell counts and a marked decrease in erythrocyte counts and haemoglobin content. Plasma aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase activities and total bilirubin concentration were higher in AlCl3 group than those of the control, while albumin and total protein concentration were significantly lower. Compared to the control, a significant raise of hepatic and erythrocyte malondialdehyde level associated with a decrease in reduced glutathione content, glutathione peroxidase, superoxide dismutase and catalase, activities of AlCl3 treated rats. However, the administration of NSO alone or combined with AlCl3 has improved the status of all parameters studied. It can be concluded that AlCl3 has induced the oxidative stress, altered the biochemical parameters and the hepatic histological profile, but the supplementation of NSO has alleviated such toxicity.

Ameliorating effects of curcumin and vitamin E on diazinon-induced oxidative damage in rat liver and erythrocytes.

The aim of this study was to evaluate the protective effects of vitamin E and/or curcumin against diazinon (DZN) (an organophosphorus insecticide)-induced toxicity of blood, liver and erythrocyte markers of male Wistar rats. The exposure of rats to DZN for 21 days provoked significant changes in red blood cell counts and hemoglobin. Results showed that lipid peroxidation increased significantly in DZN-treated rats, as evidenced by high liver and erythrocyte thiobarbituric acid reactive substance levels. Alteration of the antioxidant system in DZN-treated rats was confirmed by the significant decrease in the activity of catalase, glutathione peroxidase and glutathione-S-transferase, accompanied by a decline in reduced glutathione content in both tissues. On the other hand, a significant increase in the activities of plasma aspartate transaminase, alanine transaminase, lactate dehydrogenase and alkaline phosphatase was observed in the rats treated with DZN. However, the administration of vitamin E and curcumin has ameliorated the previous markers. In conclusion, our results indicate that the natural antioxidants like vitamin E and curcumin can effectively lower the erythrocytes and hepatic injuries induced by DZN as monitored by lipid peroxides, antioxidant enzyme activities and sensitive serum enzyme levels.

Green tea extract alleviates arsenic-induced biochemical toxicity and lipid peroxidation in rats.

The present work was undertaken to evaluate the protective effect of an aqueous extract of green tea (GT, Camellia sinensis) leaves against arsenic (NaAsO2)-induced biochemical toxicity and lipid peroxidation production in experimental rats. The treatment with arsenic exhibited a significant increase in some serum hepatic and renal biochemical parameters (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total protein, albumin, bilirubin, cholesterol, urea and creatinine). But the co-administration of GT has increased the level of plasmatic concentration of biochemical parameters. Exposure of rats to arsenic caused also a significant increase in liver, kidney and testicular thiobarbituric acid reactive substances compared to control. However, the co-administration of GT was effective in reducing its level. To conclude, our data suggest that arsenic exposure enhanced an oxidative stress by disturbing the tissue antioxidant defense system, but the GT co-administration alleviates the toxicity induced by arsenic exposure.

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.

Oxidative stress induced by thyroid dysfunction in rat erythrocytes and heart.

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 tissues were 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.

[Allergenic environment in asthmatic children in Annaba (Algeria)]. / Environnement allergénique d'une population d'enfants asthmatiques à Annaba (Algérie).

We determined blood levels of total and specific immunoglobulins E in a cohort of 75 asthmatic children at Annaba (mean age: 9 years, sex ratio M/F: 1,64). Analysis clinical investigation and biological results allowed us to estimate the clinico-biological relations in this population. We showed that: atopy based on family criteria was very frequent (74%); the symptoms of atopy associated with asthma were frequent for atopic children (96%) whose majority (46%) had severe asthma (grade 3) that required treatment. Sensitization to trophallergens was rare in this population and always associated with sensitizations to pneumallergens (acariens: 2/3; cockroaches: 50%). Sensitizations to pneumallergens seemed promoted by climatic conditions in the area of Annaba that increased the risk of developing allergic diseases.

Influence of thyroid dysfunction on liver lipid peroxidation and antioxidant status in experimental rats.

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 5 weeks by administration of 0.05% 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 gamma glutamyl transferase (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 (p<0.001), associated with a fall of the total antioxidant status (TAS) in the serum of the hyperthyroid rats. The SOD, CAT, and GPx activities in liver of hyperthyroid rats have significantly increased compared to hypothyroid rats and the controls (p<0.001). The AST, ALT, LDH, GGT, and ALP activities increased in the hyperthyroidism rats (p<0.05). 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.

The impact of thyroid activity variations on some oxidizing-stress parameters in rats.

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 rats compared to the controls, contrary to the hyperthyroidism rats, which expressed a pronounced increase. The increased glutathione peroxidase 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 superoxide 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.