OBJECTIVES: Mechanisms of the vascular effect of cadmium vary and involve nervous, hormone and intracellular signaling pathways. However, it is still not clear if mechanisms of the vascular effect of cadmium (Cd) include changes in the synthesis or release of vasoactive agents. The aim of this study was to evaluate the impact of subchronic Cd poisoning on blood nitric oxide or endothelin in blood and to relate it to the redox system activity in vessel walls and to blood Cd concentration. MATERIALS AND METHODS: The study was performed on male Buffalo rats which were given cadmium in drinking water, 50 or 200 ppm, for 12 weeks. RESULTS: The study showed different dose-dependent changes in toxicological and biochemical status. Mean serum nitric oxide concentration (measured using R&D Systems) was lower in rats poisoned with cadmium compared with the control group (57.7 +/- 7.6 vs. control 65.0 +/- 4.9 micromol/l, p < 0.05), whereas the plasma endothelin-1 level (measured using enzymoimmunoassay) and serum prostaglandin PGF2alpha concentration (determined using R&D System) were similar in all animals. The lipid peroxides concentration (measured colorimetrically) was higher in the group treated with cadmium in a dose of 50 ppm than in controls (5.2 +/- 3.0 vs. controls 1.4 +/- 0.4 nmol/ml, p < 0.001) and gluthatione concentration was decreased in the group treated with cadmium in a dose of 200 ppm as compared with the control group, (1.3 +/- 1.2 vs. control 2.5 +/- 0.9, micromol/l p < 0.05). CONCLUSIONS: It is concluded, that cadmium induces oxidative stress in both doses, however, the activity of defending mechanisms depends on Cd dose. Oxidative stress can be responsible for decreased nitric oxide concentration in serum. We suppose that the mechanisms of the vascular effect of cadmium vary and are dose-dependent. Cd used in a dose of 50 ppm for three months induces more severe functional vascular disturbances than its dose of 200 ppm.
OBJECTIVES: Mechanisms of the vascular effect of cadmium vary and involve nervous, hormone and intracellular signaling pathways. However, it is still not clear if mechanisms of the vascular effect of cadmium (Cd) include changes in the synthesis or release of vasoactive agents. The aim of this study was to evaluate the impact of subchronic Cdpoisoning on blood nitric oxide or endothelin in blood and to relate it to the redox system activity in vessel walls and to blood Cd concentration. MATERIALS AND METHODS: The study was performed on male Buffalo rats which were given cadmium in drinking water, 50 or 200 ppm, for 12 weeks. RESULTS: The study showed different dose-dependent changes in toxicological and biochemical status. Mean serum nitric oxide concentration (measured using R&D Systems) was lower in rats poisoned with cadmium compared with the control group (57.7 +/- 7.6 vs. control 65.0 +/- 4.9 micromol/l, p < 0.05), whereas the plasma endothelin-1 level (measured using enzymoimmunoassay) and serum prostaglandinPGF2alpha concentration (determined using R&D System) were similar in all animals. The lipidperoxides concentration (measured colorimetrically) was higher in the group treated with cadmium in a dose of 50 ppm than in controls (5.2 +/- 3.0 vs. controls 1.4 +/- 0.4 nmol/ml, p < 0.001) and gluthatione concentration was decreased in the group treated with cadmium in a dose of 200 ppm as compared with the control group, (1.3 +/- 1.2 vs. control 2.5 +/- 0.9, micromol/l p < 0.05). CONCLUSIONS: It is concluded, that cadmium induces oxidative stress in both doses, however, the activity of defending mechanisms depends on Cd dose. Oxidative stress can be responsible for decreased nitric oxide concentration in serum. We suppose that the mechanisms of the vascular effect of cadmium vary and are dose-dependent. Cd used in a dose of 50 ppm for three months induces more severe functional vascular disturbances than its dose of 200 ppm.