Effects Of Carbon Disulphide On Oxidation Injury And DNA Stage Of Cultured Endothelial Cells And Protects Of Vitamin C

Carbon disulfide (CS2), a volatile organic solvent, is often applied to various industry processes, such as vulcanizing rubber, fumigating grain, oil extraction, and manufacturing viscose rayon fibers. The wide use of CS2 is associated with various types of diseases. It is well known that CS2 has cardiovascular toxicity such as atherogenic effect. Chronic exposure to carbon disulfide can cause coronary heart disease hypertension and other cardiovascular disease, which has been demonstrated by many epidemiological investigations and experimental researches. Damage of endothelial cells as center of atherosclerosis is attented by many scholars. Free radicals, nitric oxide (NO) and peroxynitrite (ONOO-) have been studied as possible agents involved in the pathological changes caused by CS2. Nitric oxide plays variable physiologic and pathologic roles such as relaxation factor of endothelial cells, messenger for nerve conduction and cytotoxicity molecule in vivo. Peroxynitrite, formed as a product of nitricoxide, is extensively involved in pathologic process. Peroxynitrite causes various pathophysiological injuries in cells. The major mechanism of injury by nitric oxide in vivo is associated with the production of peroxynitrite. Peroxynitrite is the harmful consequence of increased level of nitric oxide. In addition, hyperplasia of endothelial cells is one of main pathological characteristic and is relative to free radical during initial stage and development of AS.In order to study the mechanism of atherosclerosis caused by CS2 exposure, we adopted cultured endothelial cell as biological material. 0, 10, 100, 1000, 10000 umol/L CS2 incubated with endothelial cells for 24 hours. In addition, a control group, two Vitamin C groups were set up. The concentrations of Vitamin C were 100 u,mol/L and 200 umol/L respectively. Luminol-depended chemiluminescence detected peoxynitrite anion in the cultured medium to evaluate the level of oxide. PI staining test were conducted to analyze cells ratio of DNA stage. In addition, the relation of peoxynitrite anion and cells ratio of DNA stage was analyzed.The data expressed that the level of peroxynitrite in cell culture solution with CS2 was higher than without CS2 (F=34.60,P<0.05) as well as CS2 made cells ratio of the endothelial cells in different DNA stage during cell cycle change (F=28.80, P<0.05). These followed the dose-effect dependence. 100 umol/L Vitamin C decreased the CL (P=0.000) and ratio of accumulated cells of S stage (P=0.000) caused by CS2. However, 200 umol/L Vitamin C increased the hyperplasia of endothelial cells (P=0.035) .ConclusionsThe results demonstrated that CS2 damaged directly or indirectly endothelial cells and roused peroxynitrite generating in excess. In addition, a majority of cells accumulated S stage of cell cycle after stimulated by CS2. Moderate dose Vitamin C can reduce these effects of CS2 on endothelial cells These maybe give a clew how CS2 cause AS.