Premium
Tamoxifen, protein kinase C and rat sperm mitochondria
Author(s) -
Saberwal Gurveen Sethi,
GillSharma Manjit K.,
Balasinor Nafisa,
Choudhary Jyoti,
Padwal Varsha,
Juneja H.S.
Publication year - 2003
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/s1065-6995(03)00163-x
Subject(s) - tamoxifen , sperm , sperm motility , rhodamine 123 , mitochondrion , creatine kinase , biology , endocrinology , medicine , protein kinase c , motility , lipid peroxidation , andrology , chemistry , microbiology and biotechnology , oxidative stress , kinase , biochemistry , botany , cancer , multiple drug resistance , breast cancer , antibiotics
Tamoxifen at a dose of 400 μg/kg/day has been reported to reduce the fertility of adult male rats and alter the pattern of cauda sperm motility from forward progressive to circular yawing type. Since sperm motility is powered by mitochondria, the effect of tamoxifen on mitochondrial function was studied. Tamoxifen treatment significantly increased rhodamine 123 fluorescent dye uptake by sperm mitochondria, reflecting an altered mitochondrial membrane potential. ATP and DAG levels, activities of glycolytic enzymes, creatine kinase and PKC all remained unaffected by tamoxifen. This is also the first report describing the presence of PKC α and β in rat sperm. Morphological and biochemical integrity of sperm membranes was determined by electron microscopy and malondialdehyde levels, which were unaltered after tamoxifen treatment. This study indicates that the altered sperm motility induced by tamoxifen is accompanied by changes in mitochondrial membrane potential, but in the absence of any detectable change in membrane integrity, lipid peroxidation, ATP levels and activities of glycolytic enzymes, creatine kinase and PKC.