¹Department of Biochemistry and Nutrition, Central Food Technological Research Institute, Council of Scientific and Industrial Research, Mysore, Karnataka, India

Correspondence: Dr Muralidhara, Department of Biochemistry and Nutrition, CFTRI, Council of Scientific and Industrial Research, Mysore 570 020, Karnataka, India. E-mail: mura16@yahoo.com

Received 20 December 2008; Revised 4 February 2009; Accepted 11 February 2009; Published online 12 March 2009.

Abstract

Earlier, we have shown the occurrence of oxidative impairments and their progression in the testis of diabetic adult rats. This study investigated the vulnerability of immature testis to oxidative stress and mitochondrial dysfunctions in a prepubertal (PP) diabetic rat model. PP male rats (4/6-week-old) rendered diabetic by an acute dose of streptozotocin were monitored for induction of oxidative stress in testis cytosol/mitochondria. Diabetic rats of both age groups showed severe hyperglycemia, testicular atrophy and marked oxidative damage as evidenced by enhanced generation of reactive oxygen species, hydroperoxide and malondialdehyde levels (4 week>6 week). Mitochondrial dysfunctions manifested as reduction in the activities of aldehyde dehydrogenase, tricarboxylic acid cycle enzymes, enhanced activities of oxidative phosphorylation enzymes, perturbations in calcium homeostasis and membrane potential. These evidences suggest that an immature testis is vulnerable to oxidative stress under diabetes, which may play a significant role in the development of testicular degeneration, leading to impaired fertility in adulthood.