ubiquinol and Body-Weight

Oxidative damage associated with the presence of lead (Pb) in the brain has been proposed as one possible mechanism involved in Pb toxicity. To investigate this hypothesis, we examined the long-term effects of Pb2+ on parameters of oxidative stress in the brain from rats chronically exposed to the metal (1 g Pb acetate/1 drinking water). After 8 weeks of treatment, Pb2(+)-intoxicated rats (blood Pb concentration > 100 microg/dl) showed lower body weight, and lower hematocrit and 5-aminolevulinic acid dehydratase activity as compared to controls. The content of brain 2-thiobarbituric acid-reactive substances (TBARS), an indicator of lipid oxidation, was significantly (P < 0.05) higher in the Pb2(+)-intoxicated animals than in controls. Higher activities of the antioxidant enzymes glutathione reductase and glutathione peroxidase, and a lower (44%) level of ubiquinol 10 were found in the brain of the Pb2(+)-treated rats, compared to controls. A negative correlation between brain ubiquinol 9 (r2 = 0.79), 10 (r2 = 0.84) and blood Pb concentration was observed. Brain alpha-tocopherol levels, superoxide dismutase activity and parameters of oxidative damage to proteins were similar between control and Pb2(+)-treated rats. The present results indicate that chronic Pb2+ intoxication induces an oxidative stress situation in rat brain.

Topics: Animals; Antioxidants; Body Weight; Brain; Glutathione Peroxidase; Glutathione Reductase; Hematocrit; Lead; Lead Poisoning; Lipid Peroxidation; Male; Porphobilinogen Synthase; Proteins; Rats; Rats, Wistar; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Ubiquinone; Vitamin E

Previous studies have demonstrated that zinc deficiency can be associated with high rates of oxidative damage to testes lipids, proteins, and DNA in male rats. In the present work, different aspects of the oxidant defense system (enzymes and lipid-soluble antioxidant substances) were characterized in the testes of control and zinc-deficient rats. Seventeen-day-old males were given free access to either a control (25 microg Zn/g) or a zinc-deficient (0.5 microg Zn/g) diet, or the 25 microg Zn/g diet at a level of food intake similar to that of zinc-deficient rats. Animals were sacrificed 14 days after the initiation of the diet. The activities of copper-zinc superoxide dismutase (CuZn SOD) and glutathione reductase (GRed) were significantly higher (34% and 23%, respectively) in testes from the zinc-deficient animals than in those of the ad libitum controls. In testes, the activities of manganese superoxide dismutase (Mn SOD) and glutathione peroxidase (GPx), and the concentration of alpha-tocopherol and ubiquinol-9 and -10 were similar among the groups. However, the ratio of reduced/total concentration of both ubiquinols was higher in the zinc-deficient and restrict-fed animals than in the ad libitum controls. Testes homogenates from the zinc-deficient rats showed a low susceptibility to Fe(II)-induced oxidation, which could be explained in part by a lower peroxidation index, mainly due to the decreased testicular content of the fatty acid 20:4 observed in these animals. In summary, both undernutrition and zinc-deficiency can cause an oxidative stress situation in testes, for which cells tend to compensate by increasing select components of the oxidant defense system.

Topics: Animals; Body Weight; Copper; Glutathione Peroxidase; Glutathione Reductase; Male; Organ Size; Oxidative Stress; Oxidoreductases; Phospholipids; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Superoxide Dismutase; Testis; Thiobarbituric Acid Reactive Substances; Ubiquinone; Vitamin E; Zinc