Evidence for oxidative stress at elevated plasma thiol levels in chronic exposure to carbon disulfide (CS2) and coronary heart disease

Blood oxidative stress in taiwan workers exposed to carbon disulfide

“…Workers exposed to CS 2 had significantly higher MDA levels than the controls, which is consistent with previous observations [Wronska‐Nofer et al, 2002; Wronska‐Nofer et al, 2007]. There was a significant ( P < 0.001) dose–response relationship between exposure concentration and MDA levels.…”

“…Another study [Wronska‐Nofer et al, 2002] in workers with more than 20 years of CS 2 exposure demonstrated a significant increase in MDA levels, with a concurrent decrease in antioxidants (vitamin E, SOD, GSH‐peroxidase, and catalase). A recent report [Wronska‐Nofer et al, 2007] showed that subjects exposed to CS 2 presented with increased levels of lipid oxidation products, comparable to that observed in patients with coronarographically confirmed arteriosclerotic vascular disease. However, these studies didn't examine the relationship between the levels of CS 2 exposure and the oxidative/antioxidant response.…”

“…may function as pro‐oxidants and induce oxidative modification of LDL as well as free‐radical‐dependent cytotoxicity [Starkebaum and Harlan, 1986; Munday, 1989; Jones et al, 1994]. Thus, oxidative processes occurring in subjects chronically exposed to CS 2 arise as a consequence of increased plasma thiol production [Wronska‐Nofer et al, 2002; Wronska‐Nofer et al, 2007].…”

N–nitrosamines are associated with shorter telomere length

“…Most observations for toluidines concern exposure to o-toluidine, which recently has been associated with an increased risk of bladder cancer (51) and is classified as probable carcinogen (28). CS 2 exposure is associated with increased oxidative stress (52,53), and, at least at higher exposures, with increased risk of cardiovascular diseases, health effects that also may be mediated by telomere shortening (54,55). Still, it cannot be ruled out that the effect of CS 2 in our study may be due to the fairly strong correlation to N-nitrosamines.…”

A validated HPLC‐fluorescence method with a semi‐micro column for routine determination of homocysteine, cysteine and cysteamine, and the relation between the thiol derivatives in normal human plasma

“…One of the major mechanisms of Hcy toxicity seemed to be auto-oxidation of Hcy, which reduces disulfide to free thiol, followed by the metalindependent oxidation of the free thiol to generate oxidants such as superoxide and hydrogen peroxide (Hogg, 1999). Simultaneously, other thiol derivatives such as Cys having similar chemical structure to Hcy have seemed also to be risk factors for cardiovascular disease (Kumar et al, 2006;Wronska-Nofer et al, 2007). These compounds seemed to generate reactive oxygen species during their auto-oxidation as well as Hcy.…”