Tobacco, antioxidant enzymes, oxidative stress, and genetic susceptibility in oral cancer.
OBJECTIVE
Oral cancer accounts third of all malignancies in India. Tobacco use, the major etiological factor for oral cancer is known to generate free radicals resulting in alterations in antioxidant enzymes like, glutathione-S-transferase (GST), glutathione reductase, superoxide dismutase, catalase, and glutathione peroxidase as well as lipid peroxidation and total thiol. Therefore, it is of fundamental importance to evaluate the role of tobacco and antioxidant enzymes and oxidative stress markers in oral carcinogenesis.


METHODS
One hundred forty oral cancer patients and 50 healthy controls, classified as "habitual controls" and "nonhabitual controls" having tobacco habits and no tobacco habits, respectively, were included in the study. Adjacent normal and malignant tissue samples were also collected. Erythrocyte, plasma, and tissue levels of antioxidant enzymes and total thiol were assayed by spectrophotometric methods. GSTM1 genotype was analyzed using polymerase chain reaction.


RESULTS
Antioxidant enzymes were significantly higher whereas glutathione peroxidase and thiol levels were lower in patients as compared with habitual controls. Habitual controls with higher tobacco exposure and lower antioxidant enzymes as well as thiol showed higher risk of oral cancer development. Antioxidant enzymes were higher, whereas catalase and thiol levels were lower in malignant as compared with adjacent normal tissues. Sixty-three percent of the patients showed GSTM1 null genotype.


CONCLUSIONS
The study showed risk of oral cancer development in habitual controls with lower antioxidant enzymes, lower oxidative stress markers, and higher lifetime tobacco exposure. Individuals with GSTM1 null genotype may be at higher risk of oral cancer development.
Patel
Beena P
BP
Cell Biology Division, The Gujarat Cancer and Research Institute, Asarawa, Ahmedabad, India. patel.beena@yahoo.com
Rawal
Upendra M
UM
Rawal
Rakesh M
RM
Shukla
Shilin N
SN
Patel
Prabhudas S
PS
D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000378:metabolism; D002294:Carcinoma, Squamous Cell / Q000201:enzymology / Q000235:genetics / Q000473:pathology; D016022:Case-Control Studies; D002374:Catalase / Q000378:metabolism; D020022:Genetic Predisposition to Disease; D005978:Glutathione / Q000097:blood; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000097:blood; D005982:Glutathione Transferase / Q000235:genetics*; D006801:Humans; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000175:diagnosis / Q000201:enzymology* / Q000235:genetics*; D018384:Oxidative Stress; D013438:Sulfhydryl Compounds / Q000097:blood*; D013482:Superoxide Dismutase / Q000378:metabolism; D014029:Tobacco Use Disorder / Q000201:enzymology* / Q000235:genetics* / Q000473:pathology
D000975:Antioxidants; D002374:Catalase; D005978:Glutathione; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D013438:Sulfhydryl Compounds; D013482:Superoxide Dismutase