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1 Instituto de Genética, Departamento de Biología Molecular y Genomica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, México.
2 Department of Anthropology, School of Biological & Earth Sciences, Sri Venkateswara University, Tirupati, India.
3 Instituto de Biología Molecular en Medicina, Departamento de Biología Molecular y Genomica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, México.
Address correspondence to Parvathi Kumara Reddy Thavanati, PhD, DSc, Instituto de Genética, Departamento de Biología Molecular y Genomica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Sierra Mojada 950, Puerta 7, Edificio P, Nivel II, Col. Independencia, Guadalajara. Jalisco. Código Postal: 44340. México. E-mail: tpkreddy{at}yahoo.com; reddy.parvathi{at}mail.cucs.udg.mx
To understand whether oxidants contribute to the initiation and/or promulgation toward aging, the present study has been undertaken on 220 healthy male volunteers aged 20–80 years selected from the defined electoral area (suburbs of Tirupati, Andhra Pradesh, India) to evaluate the concentrations of free radicals (superoxide anion, hydrogen peroxide), lymphocyte antioxidant enzymes (glutathione S-transferase, superoxide dismutase, catalase), and DNA damage in relation to obesity and smoking (lifestyles). A two fold increase of lymphocyte free radical generation (DNA damage) was observed in older age groups with a reduced antioxidant potential, forming a link between cigarette smoking and oxidative stress represented by an antioxidant imbalance. Body mass index had a positive relationship with oxidative stress, but antioxidant levels did not vary with body mass index. The findings conclude that free radical–mediated oxidative stress and DNA damage accelerate with lifestyle variations under reduced antioxidant potential.
Key Words: Aging Antioxidants DNA damage Smoking Obesity
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