title: Evidence for oxidative stress at elevated plasma thiol levels in chronic exposure to carbon disulfide (CS2) and coronary heart disease.
abstract: OBJECTIVE
  Oxidative stress in plasma may be promoted by plasma thiols such as homocysteine. However, other thiols such as glutathione may also exert antioxidant effects in vitro and in vivo. To further investigate whether plasma thiols act as prooxidants or antioxidants, we compared plasma oxidative status in patients with coronary heart disease (CHD) and in subjects occupationally exposed to carbon disulfide (CS(2)).
  
  
  METHODS
  Fifty-five subjects chronically exposed to CS(2), 53 CHD patients, and 52 healthy controls were examined. To assess plasma oxidative status, concentrations of thiobarbituric reactive substances (TBARS) and total antioxidative capacity (TAC), as well as ferritin and ceruloplasmin were determined. Antioxidative reserve was assessed by the determination of vitamine E, uric acid, superoxide dismutase, catalase, and glutathion peroxidase. In addition, protein and non-protein plasma thiol levels were measured.
  
  
  RESULTS
  Patients in both groups had increased levels of plasma thiols as compared to controls: CS(2)-exposed subjects presented with increased levels of thiols associated with plasma proteins, whereas CHD patients presented with elevated total homocysteine and cysteine levels. TBARS were significantly increased and TAC was significantly decreased both in CS(2)-exposed subjects and in CHD patients. In addition decreased activity of glutathione peroxidase, an antioxidative enzyme inhibited by thiol-containing compounds, was noted in both groups.
  
  
  CONCLUSIONS
  These results demonstrate that regardless of their metabolic origin increased thiols are associated with increased oxidative stress in plasma.
authors.affiliation: Department of Biochemical Toxicology, Nofer Institute for Occupational Medicine, Lodz, Poland.
authors.forename: Teresa
authors.initials: T
authors.lastname: Wronska-Nofer
authors.forename: Jerzy-Roch
authors.initials: JR
authors.lastname: Nofer
authors.forename: Jan
authors.initials: J
authors.lastname: Stetkiewicz
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Wierzbicka
authors.forename: Halina
authors.initials: H
authors.lastname: Bolinska
authors.forename: Manfred
authors.initials: M
authors.lastname: Fobker
authors.forename: Helmut
authors.initials: H
authors.lastname: Schulte
authors.forename: Gerd
authors.initials: G
authors.lastname: Assmann
authors.forename: Arnold
authors.initials: A
authors.lastname: von Eckardstein
mesh_terms: D000328:Adult; D002246:Carbon Disulfide / Q000009:adverse effects*; D016022:Case-Control Studies; D002570:Ceruloplasmin / Q000378:metabolism; D003327:Coronary Disease / Q000209:etiology / Q000378:metabolism*; D005293:Ferritins / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D016273:Occupational Exposure / Q000009:adverse effects; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D013438:Sulfhydryl Compounds / Q000097:blood*; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis*
chemical_list: D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; D005293:Ferritins; D005979:Glutathione Peroxidase; D002570:Ceruloplasmin; D002246:Carbon Disulfide