Nicotine Enantiomers and Oxidative Stress

Abstract

Nicotine affects a variety of cellular processes ranging from induction of gene expression to secretion of hormones and modulation of enzymatic activities. The objective of this study was to characterize the toxicity of nicotine enantiomers as well as their ability to induce oxidative stress in an in vitro model using Chinese hamster ovary (CHO) cells. Colony formation assay has demonstrated that (−)-nicotine is the more toxic of the enantiomers. At 6 mM concentrations, (−)-nicotine was found to be ≈28- and 19-fold more potent than (+)-, and (±)-nicotine (racemic), respectively. Results also indicated that the toxicity of (±)-nicotine is higher than that of (+)-nicotine. (−)-Nicotine at a 10 mM concentration substantially decreased glutathione (GSH) levels (46% decrease). In addition, a 3-fold increase in malondialdehyde (MDA) level was evident in cells after exposure to 10 mM (−)-nicotine. Increased lactate dehydrogenase (LDH) activities in the media demonstrated that cellular membrane integrity was disturbed in nicotine treated cells. In the presence of superoxide dismutase (SOD) and catalase (CAT), the LDH activities returned to control value in 24 h with all concentrations of (−)-, (+)-, and (±)-nicotine. The decreases in LDH activities in the presence of the radical scavenging enzymes SOD and CAT suggest that membrane damage may be due to free radical generation.

Department(s)

Chemistry

International Standard Serial Number (ISSN)

0300-483X

Document Type

Article - Journal

Document Version

Citation

File Type

text

Language(s)

English

Rights

© 1998 Elsevier, All rights reserved.

Publication Date

01 Sep 1998

Link to Full Text

Share

 
COinS