Subchronic inhalation of particulate matter 10 coal dust induces atherosclerosis in the aorta of diabetic and nondiabetic rats

Abstract

This study aimed to elucidate whether subchronic inhalation of particulate matter (PM10) coal dust induces atherosclerosis in diabetic rats. A total of 32 male Wistar rats, were randomly divided into eight groups including four nondiabetic groups and four groups of diabetic rats. These rats were exposed to doses of coal dust equal to 0 mg/m3, 6.25 mg/m3, 12.5 mg/m3, or 25 mg/m3 for 1 hour/day for 28 days. Plasma levels of lipid peroxides were determined as thiobarbituric acid reactive substance. The levels of circulating endothelial cells were analyzed histologically. Foam cells formation was analyzed in aorta and tail artery with Oil Red O staining. Analysis of variance test was used to compare all parameters. Nondiabetic rats exposed to coal dust had significantly increased oxidative stress compared to the control group (p < 0.05). Diabetic rats exposed to coal dust at dose of 25 mg/m3 had significantly increased oxidative stress compared to that of control diabetic rats (p < 0.05). The levels of endothelial damage were significantly increased in diabetic rats exposed to coal dust at doses of 6.25 mg/m3 and 12.5 mg/m3 (p < 0.05) compared to control diabetic rats. The foam cell counts were significantly increased in the aorta of nondiabetic rats exposed to coal dust at doses of 6.25 mg/m3 and 25 mg/m3 compared to control rats (p < 0.05), also in the tail artery at dose of 25 mg/m3. The foam cell counts were significantly increased in the aorta of diabetic rats exposed to coal dust at doses of 6.25 mg/m3 and 12.5 mg/m3 than that in control diabetic rats (p < 0.05). Subchronic inhalation of PM10 coal dust induces atherosclerosis through oxidative stress and endothelial damage in aorta of nondiabetic and diabetic rats.