Abstract: Selenium (Se) is involved in the process of male reproduction.
Several studies have been carried out to find the mechanism of Se action
through identified selenoproteins. Especially selenoenzyme phospholipid
glutathione peroxidase (PHGPx, GPx-4) plays a pivotal role in regulating
spermatogenesis. However, the action of selenium is best known as an
antioxidant which acts through various selenoproteins viz. glutathione
peroxidase, thioredoxin reductase and selenoprotein P. Oxidative stress is
currently being considered a leading cause of male infertility. Presently, the
involvement of redox active transcription factor, AP1 (Activator protein1) in
testicular function was studied. AP1 is redox sensitive and also controls cell
proliferation. The effects of Se might be mediated through it. Different Se
status – deficient, adequate and excess Se – were generated in male Balb/c
mice by feeding yeast based selenium deficient diet and deficient diet
supplemented with Se as sodium selenite (0.2 and 1 ppm Se), respectively, for a
period of 4 and 8 weeks. Se status was checked by measuring the Se levels and
glutathione peroxidase (GSH-Px) activity in testis and liver. The reproductive
potential of mice was affected at these changed Se levels. Changes in the
activity of superoxide dismutase (SOD), levels of reduced glutathione (GSH) and
oxidized glutathione (GSSG) were observed indicating increased oxidative stress
at both the levels. Further, changes in the mRNA expression of GSH-Px,
γ-glutamylcysteine synthetase
γGCS) and Mn superoxide dismutase (MnSOD) were
observed. Decrease in cjun and cfos mRNA levels were observed at both the
Se status (deficient and excess) which might be responsible for decreased germ
cell number, differentiation and reduced fertility observed at the altered Se
levels.
Keywords: Testes, cjun, cfos, RT-PCR, selenium
Journal: BioFactors, vol. 23, no. 3, pp. 151-162, 2005
