ZHANGRUI; ZHONGLAI－FU; 等
The present study was performed to determine the influence of lipid peroxidation and perturbance of Ca2+ homeostasis on liver damage induced by 2-chloro-1,3-butadiene(CBE)and the protective effects of vitamin E in Wistar rats.Animals were given intraperitoneally different doses(8,40 or 200mg·kg-1 daily)of CBD for 21 days,and the following dose-dependent events were observed;liver damage,significant increase in liver lipid peroxides,and decreases in activities of erythrocytic glutathione peroxidase(GSH-Px) and superoxide dismuatase(SOD).The pretreatment of rats with vitamin E(po 150mg·kg-1)before administering CBD(iP 60mg·kg-1)daily for 21 days prevented the following CBD-induced changes,the increase in serum cholylglycine(CG),hepatic LP,hepatic mictochondrion LP,hepatic oxidized glutathioe(GSSG)(while the significant increase of reduced glutathione(GSH)was not affected)and the decrease in activities of erythrocytic SOD and hepatic mitochondrial calcium sequestration.These results suggest that lipid peroxidation and perturbance of Ca2+ homeostasis appear to comtribute to the hepatotoxicity of CBD,and vitamin E might prevent the liver damage induced by CBD.The decrease in activities of GSH-Px and SOD in erythrocytes might be used as biomarkers for adverse effects of CBD on defense sytem against lipid peroxidation.
Mast, T.J.; Evanoff, J.J.; Westerberg, R.B.; Rommereim, R.L.; Weigel, R.J.
Chloroprene, 2-chloro-1,3-butadiene, is a colorless liquid with a pungent ethereal odor that is primarily used as an intermediate in the manufacture of neoprene rubber, and has been used as such since about 1930. This study addressed the potential for chloroprene to cause developmental toxicity in New Zealand white rabbits following gestational exposure to 0, 10, 40, or 175 ppm chloroprene vapors, 6h/dy, 7dy/wk. Each treatment group consisted of 15 artificially inseminated females exposed on 6 through 28 days of gestation (dg). Body weights were obtained throughout the study period, and uterine and fetal body weights were obtained at sacrifice on 29 dg. Implants were enumerated and their status recorded and live fetuses were examined for gross, visceral, skeletal, and soft-tissue craniofacial defects. There were no overt signs of maternal toxicity and the change in maternal body weight over the course of the study was not affected. Exposure of pregnant rabbits to chloroprene vapors on 6-28 dg had no effect on the number of implantation, the mean percent of live pups per litter, or on the incidence of resorptions per litter. The incidence of fetal malformations was not increased by exposure to chloroprene. Results of this study indicate that gestational exposure of New Zealand white rabbits to 10, 40, or 175 ppm chloroprene did not result in observable toxicity to either the dam or the offspring.