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Impairment of cell and plasma redox state in subjects professionally exposed to chromium
Author(s) -
Mattia Giancarlo De,
Bravi Maria Cristina,
Laurenti Oriana,
Luca Orietta De,
Palmeri Alessandro,
Sabatucci Antonio,
Mendico Gino,
Ghiselli Andrea
Publication year - 2004
Publication title -
american journal of industrial medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.7
H-Index - 104
eISSN - 1097-0274
pISSN - 0271-3586
DOI - 10.1002/ajim.20044
Subject(s) - ascorbic acid , glutathione , oxidative stress , antioxidant , chromium , redox , thiobarbituric acid , thiol , medicine , endocrinology , chemistry , biochemistry , lipid peroxidation , inorganic chemistry , food science , organic chemistry , enzyme
Background Chromium (Cr) is widely used in chemical, tannery, building, and metal industries. More recently, it has been demonstrated that Cr induces oxidative stress in mouse brain. Nevertheless very few data exist on in vivo oxidative damage in humans exposed to Cr. Methods Changes in antioxidant parameters both in plasma (acid ascorbic redox state and total antioxidant capacity) and in red blood cells (glutathione (GSH) redox state) of 40 subjects (age 37.65 ± 7.46; M/F 20/20) professionally exposed to Cr who were recruited from metal, chemistry, and building industries were evaluated. We also evaluated the levels of lipoperoxidation (thiobarbituric acid‐reactive material, TBA‐RM) and thiol levels in plasma to assess the extent of oxidative stress state. To evaluate Cr exposure rate, we measured urinary‐chromium (U‐Cr) by an electrothermic atomization‐atomic absorption spectrometry (ETA‐AAS) method. Results In this study, we found that Cr exposure induced a decrease both in GSH ( P < 0.0005) and GSH/oxidized glutathione (GSSG) ratio ( P < 0.0001) in red blood cells from workers with respect to control subjects. Furthermore, we also demonstrated a significant decrease of plasma acid ascorbic levels (45.7 ± 14.9 vs. 53.5 ± 16.5 μmol/L; P < 0.05) and in total plasma antioxidant capacity (1,126.3 ± 212.2 vs. 1,266.9 ± 207.8 μmol/L; P < 0.05) in subjects exposed to Cr. No difference was found with regard to TBA‐RM and thiol levels. Conclusions This study demonstrated that in humans, an oxidative stress occurs for Cr exposures as low as those considered safe. This oxidative stress appears to be able to affect intracellular and plasmatic antioxidant defense. Am. J. Ind. Med. 46:120–125, 2004. © 2004 Wiley‐Liss, Inc.