Increased oxidative stress in subjects exposed to carbon disulfide (CS2)--an occupational coronary risk factor.

There is considerable epidemiological evidence that workers exposed to carbon disulfide (CS2) develop premature atherosclerosis leading to increased rates of coronary heart disease (CHD), but mechanisms underlying this association remain obscure. The present study documents that occupational exposure to CS2 modifies the oxidative status of plasma, which is a major determinant of the susceptibility to atherosclerosis. Concentrations of thiobarbituric reactive substances (TBARS), which reflect lipid peroxidation processes in plasma, were determined in 29 men who were exposed to CS2 for more than 20 years, in 24 patients with peripheral atherosclerosis, and in 30 unexposed, healthy control subjects.

Genotoxicity of industrial dyes under the inductive effect of ethanol on monooxygenase system in mice.

The genotoxic effects of triarylmethane (Acid Green 16, C.I.44025) and arylmonoazo (Basic Orange 28, developed by Boruta Pigment Plant, Poland, C.

Cytochrome P-450 mediated genotoxicity of triarylmethane dye in mice fed ethanol liquid diet.

Genotoxic effect of synthetic triarylmethane dye (Acid Green 16) was evaluated in Balb C mice fed nutritionally adequate liquid diet (1 kcal/ml) or isocaloric alcoholic diet containing 5% (w/v) ethanol (36% of total calories) for 6 days. Dye compound was given intraperitoneally at dose 150 mg/kg body wt. 30 h before test.

Toxic effects of subchronic combined exposure to n-butyl alcohol and m-xylene in rats.

Effects of combined exposure to m-xylene and n-butyl alcohol in the conditions of subchronic inhalation experiment in rats were examined. Rats were exposed to vapours of individual solvents at concentrations of 50 and 100 ppm and their 1:1 mixture at concentrations of 50 + 50 ppm and 100 + 100 ppm, 6 h/day, 5 days/week for 3 months. No significant changes in body weight gain, in absolute and relative organ weights and clinical biochemistry parameters were observed.

Biological markers of oxidative stress induced by ethanol and iron overload in rat.

Studies on rats treated for 15 months with ethanol (10%, w/v, solution in drinking water) revealed that the stimulation of hepatic cytochrome P-450 monooxygenases activity was accompanied by enhanced microsomal malondialdehyde formation, a lipid peroxidation index and a decreased level of the antioxidant, alpha-tocopherol. The other components of the prooxidant/antioxidant system, diene conjugates and catalase, glutathione peroxidase and superoxide dismutase activities were unaffected. Oxidative stress in blood was shown by a significant decrease in the alpha-tocopherol level whereas lipid peroxidation and antioxidant enzyme activity remained unchanged.