Open AccessSpermatotoxic effects of galactose and possible mechanisms of action
Author(s) -
Toyin Muhammed Salman,
Luqman Aribidesi Olayaki,
Isiaka Abdullateef Alagbonsi,
Adeoye Oyetunji Oyewopo
Publication year - 2016
Publication title -
middle east fertility society journal/middle east fertility society journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.322
H-Index - 18
eISSN - 2090-3251
pISSN - 1110-5690
DOI - 10.1016/j.mefs.2015.09.004
Subject(s) - luteinizing hormone , galactose , endocrinology , sperm , medicine , hormone , follicle stimulating hormone , sperm motility , testosterone (patch) , catalase , toxicity , oxidative stress , superoxide dismutase , biology , lactate dehydrogenase , andrology , chemistry , biochemistry , enzyme
While numerous studies have documented the ovotoxic effect of galactose, few available studies on male gonad are of the opinion that it seems to fully escape the toxic effects galactose exerts on the ovary. The present study was therefore designed to further investigate the effects of galactose on male sperm parameters and some reproductive hormones. Thirty male albino rats (200–250 g) were randomly divided in a blinded fashion into 6 groups (n = 5). Group A received normal saline and served as control. Groups B, C, D, E and F received 3 mg/kg, 10 mg/kg, 20 mg/kg, 30 mg/kg, and 40 mg/kg of galactose respectively through oral gavage for 42 days. The results showed that chronic administration of galactose promotes sperm toxicity by reducing epididymal sperm count, motility and percentage of morphologically normal sperm. Moreover, galactose increased luteinizing hormone but slightly decreased testosterone and had no effect on follicle stimulating hormone. Galactose also caused a slight decrease in superoxide dismutase and increase in lactate dehydrogenase activity but no effect on catalase. The present study thus showed that chronic administration of galactose could promote sperm toxicity which could be mediated partly by oxidative stress. Moreover, the response of the hormones is similar to that in premature ovarian insufficiency (POI) in female galactosemic model