PubMed · 8008529
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B Gaston, J F Keith. 1994. Nitric oxide and bleeding time.. https://pubmed.ncbi.nlm.nih.gov/8008529/
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There is growing epidemiological evidence for statistical associations between increases in air pollution, especially particulate matter, and increases in cardiovascular morbidity and mortality. Laboratory studies have shown that transition metals contribute strongly to the effects of high lung doses of model particles on changes in the electrocardiograms of animals. The present study evaluated the effects of short-term inhalation exposure to respirable particles of specific oxide and sulfate forms of transition metals on heart rate and the electrocardiogram of old dogs having preexisting cardiac abnormalities. Conscious beagle dogs were exposed by oral inhalation for 3 h on each of 3 successive days to aerosols of manganese, nickel, vanadium, iron, and copper oxides, and nickel and vanadium sulfates as single compounds at concentrations of 0.05 mg/m(3). Electrocardiograms were recorded and evaluated for exposure-related changes in heart rate, heart rate variability, and abnormalities of waveforms. Although the electrocardiograms of this population of dogs having potential age and cardiovascular susceptibility factors reflected their underlying clinical abnormalities, no significant effect of exposure to the transition metal aerosols was observed.
Effects of exposure to sulfur dioxide (SO(2)) on levels of thiobarbituric acid-reactive substances (TBARS), levels of reduced glutathione (GSH), and the activities of Cu,Zn-superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) were investigated in stomachs and intestines of Kunming albino mice of both sexes. SO(2) exposure at different concentrations (22, 56, and 112 mg/m(3)) was administered to the animals of SO(2) groups in the exposure chambers for 6 h/day for 7 days, while control groups were exposed to filtered air under the same condition. Our results show that SO(2) caused lipid peroxidation and changes of antioxidative status in stomachs and intestines of mice. Exposure to SO(2) at all concentrations tested caused significantly the increase of TBARS levels in stomachs and intestines of mice. For the stomachs, activities of these antioxidant enzymes and levels of GSH were significantly unaltered by SO(2) at low concentrations, except significant increase of SOD activity in the stomachs of male mice. However, higher SO(2) caused the significant increases of CAT activities and the significant decreases of GSH levels and activities of SOD and GPx. For intestines, SO(2) at all concentrations tested decreased significantly activities of SOD relative to control animals; SO(2) caused the decreases of GPx activities, but only the decreases of GPx activities caused by SO(2) exposures at higher concentrations (56 and 112 mg/m(3)) were statistically significant. SO(2) at all concentrations tested tended to increase the CAT activities in a dose-dependent manner, but the decreases of CAT activities caused by higher SO(2) were significant. SO(2) at all concentrations tested decreased significantly levels of GSH in intestines of both sexual mice. These results lead to conclusion that SO(2) exposure can caused oxidative damage to stomachs and intestines of mice, and SO(2) is a toxic agent to stomachs and intestines of mammals, not only to respiratory system. Further work is required to understand toxicological role of SO(2) on multiple or even all organs in human and animal.
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