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As nitrogen metabolism is exacerbated during diabetes mellitus or/and pregnancy, and because arginase catalyses the arginine hydrolysis into ornithine and urea, this enzyme activity as well as the ornithine content were investigated in tissues (liver, kidney and brain) from pregnant or non pregnant streptozotocin (STZ) diabetic rats, dietary supplemented or not with antioxidant vitamins (C and E). Sixty 12 week old female Wistar rats were randomly divided into 6 equal groups according to their gestational status and the dietary treatments. The groups 1 (non pregnant) and 2 (pregnant) received only intraperitoneal injection of citrate buffer and served as controls, whereas the animals of the groups 3 (non pregnant) and 4 (pregnant) were treated with STZ (40 mg/kg) and those of the groups 5 (non pregnant) and 6 (pregnant) were submitted to STZ administration and to a dietary combined ascorbate and -tocopherol acetate (1 g and 600 mg/kg food respectively) supplementation for 20 days. Except for the kidneys from not supplemented diabetic rats in which the arginase activity and the ornithine content were significantly increased in pregnant rats, no significant difference was evidenced between pregnant and non pregnant females. The arginase activity and the ornithine content were dramatically enhanced in the liver of diabetic animals (pregnant or not) (p

We tested the effects of various antioxidants on H2O2- induced TRPM2 cation channel currents. CHO cells were transfected with cDNA coding for TRPM2. The antioxidants glutathione, vitamins C and E were applied either extracellularly or intracellularly. Non-selective cation currents in whole cell experiments were consistently induced by intracellular ADP- ribose, NAD and extracellular H2O2. ADP-ribose and NAD was characterized a slow current induction to a plateau although the inward currents of H2O2 administration did not reach a plateau after even 15-20 min. No intracellular antioxidants prevented the H2O2- induced current development in whole and single-channel activities of the cells. We concluded that non reversible the selective cation channel currents induced by H2O2 although the antioxidants have no effects on the activation.

We determined the effects of intraperitoneally administered vitamin C on the lipid peroxidation (as thiobarbituric acid-reactive substances, TEARS) and vitamin C and E levels and reduced glutathione (GSH) and glutathione peroxidase (GSH-Px) activity in the plasma, red blood cells (RBC), liver, and muscle of rats in relation to oxidative damage associated with diabetes induced by streptozotocin (STZ). One group was used as control and a second as diabetic. A third group received 30 mg vitamin C i.p. every other day. On day 4 after the injection of vitamin C, animals in the second and third groups were made diabetic by i.p. injection of STZ and administered vitamin C for 21 consecutive days, and we determined TEARS, vitamin E, and GSH levels and GSH-Px activities in plasma, RBC, liver, and muscle samples. Vitamin E levels in the plasma and liver were significantly higher (P < 0.05) in the control group than in the diabetic group. Also, TEARS levels in the plasma, REC, liver and muscle samples were significantly lower (P < 0.05) in controls than in the diabetic group. The TEARS levels in the RBC, liver, and muscle samples of the vitamin C group were significantly lower (P < 0.05, P < 0.01, and P < 0.001, respectively). However, GSH-Px and GSH activities in RBC, liver, and muscle and vitamin C levels in liver were not significantly different between control and diabetic groups. Vitamin E levels in plasma (P < 0.05, P < 0.01) and liver (P < 0.001), vitamin C levels in liver (P < 0.001), and GSH (P < 0.01) and GSH-Px activities in RBC (P < 0.05, P < 0.01) were significantly higher in the vitamin C group than both the control and diabetic groups. These results indicate that vitamin C has significant protective effects on the blood, liver, and muscle of rats against oxidative damage in diabetes.

It is well known that oxidative stress damages bimolecules such as DNA and lipids. No study is available on the morphine-induced oxidative damage and fatty acids changes in brain and spinal tissues. The aim of this work was to determine the effects of morphine on the concentrations and compositions of fatty acid in spinal cord segments and brain tissues in rabbits as well as lipid peroxidation (LP) and glutathione (GSH) levels in cortex brain. Twelve New Zealand albino rabbits were used and they were randomly assigned to two groups of 6 rabbits each. First group used as control although morphine administrated to rats in second group. Cortex brain and (cervical, thoracic, lumbar) samples were taken. The fatty acids between n:18.0 and 21.0 were present in spinal cord sections and n:10 fatty acids in control animals were present in the brain tissues. Compared to n:20.0-24.0 fatty acids in spinal cord sections and 8.0 fatty acids in the brain tissues of drug administered animals. The concentration and composition of the fatty acid methyl esters in spinal cord and brain tissues was decreased by morphine treatments. LP levels in the cortex brain were increased although GSH levels were decreased by the morphine administration. In conclusion, unsaturated fatty acids contents in brain and spinal cord sections and GSH were reduced by administrating spinal morphine although oxidative stress as LP increased. The inhibition oxidative damage may be a useful strategy for the development of a new protection for morphine administration as well as opiate abuse. © 2006 Springer Science+Business Media, LLC.