ABSTRACT
Objective To investigate the effect of subchronic inhalation of toluene diisocyanate (TDI) on oxidative stress damage in rat lung tissue. Methods SPF-grade Sprague-Dawley male rats were randomly divided into 4 groups,the rats were placed in a HOPE-MED 8050A movable poison cabinet in a cage.To observe the ultrastructural and histopathology changes of lung tissue in rats.The levels of reduced glutathione (GSH), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) in lung tissue were detected. The ultrastructural and histopathological changes were examined. The expression levels of HO-1 mRNA and protein were detected by Real-time PCR and Western Blot, respectively. Results The body mass, lung tissue mass, and lung organ coefficient of rats in each dose group were lower than those in the control group (P0.05). Conclusion Subchronic inhalation of TDI can cause changes in the pathology and ultrastructure of rat lung tissue, leading to abnormal levels of metabolic enzymes in lung function, thereby inducing oxidative stress damage to the lungs. However, but HO-1 is involved in oxidative stress damage in the lungs induced by TDI.
ABSTRACT
Objective To investigate the effect of subchronic inhalation of toluene diisocyanate (TDI) on the pathological changes, oxidative stress damage, and HO-1 expression levels in rat liver tissues. Methods Forty healthy 3-week-old SPF-grade Sprague-Dawley male rats were randomly divided into 4 groups (control group, low-dose group, medium-dose group, and high-dose group), each with 10 rats. The rats were placed in a HOPE-MED 8050A movable poison cabinet in a cage. TDI was administered to animals by inhalation at doses of 0, 3.06 mg/m3, 12.25 mg/m3, and 49.00 mg/m3, respectively, for 6 hours a day and 5 days a week, and continuously for 13 weeks. The control group was exposed to fresh air. The effect of TDI on pathological changes, oxidative stress damage and HO-1 expression in rat liver tissues was examined. Results Compared with the control group, the rats in the medium and high-dose TDI-exposed groups exhibited vacuolar changes, hepatocyte swelling, steatosis and other pathological changes. With the increase of the TDI dose, the gap between hepatocytes was widened, mitochondria were swollen and vacuolated, and mitochondrial cristae disappeared. The expression levels of HO-1 gene and protein in the liver tissues of the low, medium, and high dose groups were significantly higher than those in the control group (P<0.05). Compared with the control group, the number of HO-1 positive cells in the low, medium and high dose groups increased and the staining increased gradually, and the difference was statistically significant (P<0.05). Conclusion TDI exposure can cause oxidative damage to rat liver tissues and induce the expression levels of HO-1 gene and protein expression.
