Effect of cadmium and aluminum intake on the antioxidant status and lipid peroxidation in rat tissues.

This work aimed to study the relationship between the accumulation of cadmium (Cd) or aluminum (Al) in certain tissues and the levels of lipid peroxides as well as tissue antioxidants. To carry out such investigations, CdCl2 was given to rats in two dose levels; 0.5 or 2.0 mg/kg i.p for 1 day or daily repeated doses for 2 weeks. Al was given as AlCl3 either in a single dose of 100 mg/kg or daily repeated doses of 20 mg/kg for 2 and 4 weeks. The measured parameters were tissue malondialdehyde (MDA, index of lipid peroxidation) and reduced glutathione (GSH) levels as well as the activities of glutathione peroxidase (GSH-PX), glutathione reductase (GSSG-R), and glucose-6-phosphate dehydrogenase (G-6-PDH) enzymes. Liver and kidney functions were assessed by measuring serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities as well as serum urea and creatinine concentrations. Cd and Al concentrations in the studied tissues were also measured. Results indicated that tissue Cd was significantly increased after administration of either Cd doses. After a single dose of 0.5 or 2.0 mg/kg CdCl2, the increase in tissue Cd levels were accompanied by an increase in MDA and a decrease in GSH levels. On the other hand, after repeated administration of Cd, tissue Cd accumulation was accompanied by increased hepatic and renal GSH levels with decrease in MDA content and a decrease in GSH-PX activity in liver. Liver function was affected at all dose regimens, whereas kidney function was affected only after 2 weeks administration of the higher dose. In Al treated rats, Al concentration was shown to be increased in liver much more than in brain. This was accompanied by a slight decrease in hepatic GSH level after 2 weeks and a decrease in GSH-PX activity after 4 weeks. Liver function was affected only after repeated injection of Al for 2 or 4 weeks. In general, Al administration exhibited safer pattern than Cd.

Antioxidant effect of N omega-nitro-L-arginine methyl ester (L-NAME) on global cerebral ischemia in a rat model.

The antioxidant effect of the non-specific nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (CAS 50903-99-6, L-NAME), was studied in a rat model of global cerebral ischemia. In addition, the influence of low doses of L-NAME on nitric oxide production, measured as nitrate/nitrite end products, was investigated in the ischemic rats. Ischemia was induced by bilateral clamping of the common carotid arteries for 60 min followed by a reperfusion period for 60 min. L-NAME was administered intraperitoneally in the doses of 1 and 3 mg kg-1, twice, immediately after ischemia and 15 min before termination of the experiment. The drug decreased the elevated activity of lactate dehydrogenase (LDH, 1.1.1.27) as well as the increased level of lipid peroxide in the rat brain. L-NAME was also capable to normalize the reduced activity of superoxide dismutase (SOD, 1.15.1.1) that was observed after ischemia. Improvement of these parameters in L-NAME-treated rats was parallel to normalization of nitric oxide production in the treated animals. These results indicate that inhibition of nitric oxide synthase, induced by L-NAME, could improve the oxidative status of the rat brain after ischemia.

Nicotine and stress: effect on sex hormones and lipid profile in female rats.

This work aimed to study the changes in sex hormones and lipid profile in adult female albino rats subjected to treatment with nicotine (N), immobilization stress (S), or their combinations (N+S). These treatments were applied either for one day (T1) or daily for 10 days (T10), after which rats in the estrus stage were used for the determination of plasma corticosterone (CS), serum sex hormones as progesterone (P), estrogen (E), FSH, LH and serum lipid profile including total cholesterol (TC), HDL-C, LDL-C, triacylglycerol (TG) and non esterified fatty acids (NEFA). It was clear that either N or S raised plasma CS and serum P levels in both the treatment regimens and that N+S induced a higher level of these hormones compared to each treatment alone. Serum E level was only elevated during T10 regimen only. An increase in serum LH level was only observed after a single exposure to either N or S, however their combination abolished the stimulatory effect induced by each treatment alone. Serum FSH was not altered by exposure to either N or S alone in both regimens, but in the T10 regimen their combination significantly lowered FSH level. Regarding the effect on serum lipid profile, serum TC was increased in all T10 regimen groups. LDL-C was increased by N+S treatment in both regimens, however no change in HDL-C level was observed in all groups. Serum NEFA was increased in all the treated groups during T10 regimen, while in the T1 regimen NEFA level was only elevated by the combination N+S. Serum TG was insignificantly altered in all the treated groups. The observed changes in the lipid pattern were attributed to the alterations occurred in CS and female sex hormones that caused by N, S or their combinations.

Effect of pumpkin-seed oil on the level of free radical scavengers induced during adjuvant-arthritis in rats.

Pumpkin-seed oil (PSO), a natural supplement rich with antioxidant ingredients, was given to rats in which arthritis was induced using Freund's complete adjuvant. Its effect was compared with that of indomethacin, as a classical anti-inflammatory agent. Two experimental patterns were studied, an acute phase that was applied only with PSO and a chronic phase applied for both PSO and indomethacin. Compared to normal untreated rats, it was shown that the induction of arthritis caused a decrease in serum sulphhydryl groups, with an increase in serum ceruloplasmin in both phases. Blood glutathione was first elevated in the acute phase, then its level was reduced in the chronic phase. Serum N-acetyl-beta-D-glucosaminidase activity was elevated only at the acute phase, while plasma total proteins and albumin were reduced at the chronic phase. Liver glucose-6-phosphate dehydrogenase activity was markedly increased, while no changes were observed in the levels of liver lipid peroxides and glutathione. These changes in the studied parameters were attributed to the superoxides and free radicals during arthritic inflammation. Administration of PSO succeeded in modulating most of the altered parameters affected during arthritis, especially at the chronic phase. Also, a remarkable inhibition of paw oedema was observed. A similar pattern was obtained upon treatment with indomethacin except that indomethacin markedly elevated liver lipid peroxides levels. Concurrent administration of PSO with indomethacin caused no changes in the parameters studied compared to that induced by treatment with indomethacin alone.

Effect of praziquantel on some aspects of carbohydrate metabolism in mice infected with Schistosoma mansoni.

Schistosoma mansoni infection in mice resulted in a marked decrease in blood glucose and liver glycogen accompanied by a significant increase in hepatic glucose-6-phosphatase (G-6-Pase) activity. Moreover, the results indicated that infection produced a significant increase in blood pyruvate and hepatic glucose-6-phosphate dehydrogenase (G-6-PD) activity with a significant decrease in blood lactate. Infected mice were treated with praziquantel which was given at two doses of 500 mg/kg body wt on two consecutive days. Seven and 14 days respectively after drug administration, such treatment caused a marked improvement in the previous aspects of carbohydrate metabolism. This is indicated by the tendency of the blood glucose of infected mice to be restored, the marked increase in their liver glycogen content, the normalization of their blood lactate and pyruvate as well as by the marked decrease of their hepatic G-6-Pase activity and the progressive increase in their hepatic G-6-PD activity. Praziquantel given to normal mice moderately affected the blood glucose and the previously mentioned hepatic enzymes. However, the drug markedly increased the liver glycogen content of normal mice and failed to elicit any change in their blood pyruvate and lactate. Possible explanations of these findings are discussed.

Effect of chronic administration of DL-amphetamine and fenfluramine on adrenocortical functions and on certain aspects of carbohydrate and fat metabolism.

Chronic treatment of rats with amphetamine (4 mg/kg body mass) or fenfluramine (10 mg/kg body mass) might have stimulating effects on adrenocortical function. This was indicated by the significant decrease in adrenal cholesterol, ascorbic acid, glycogen, and the increase in adrenal phosphorylase activity. Both 17-oxo (17-OS) and 17-hydroxy-corticosteroids (17-OHS) were also increased by fenfuramine, while only 17-OHS was increased by amphetamine. Amphetamine did not affect plasma glucose, liver glycogen and phosphorylase activity, while fenfluramine increased liver glycogen but did not affect plasma glucose or liver phosphorylase activity. The drugs markedly increased plasma free fatty acids (FFA) which might indicate increased lipolysis.