Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Cell Physiol 254: C564-C570, 1988;
0363-6143/88 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Reyes, J.
Right arrow Articles by Benos, D. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reyes, J.
Right arrow Articles by Benos, D. J.

AJP - Cell Physiology, Vol 254, Issue 4 C564-C570, Copyright © 1988 by American Physiological Society


ARTICLES

A bioenergetic model of gossypol action: effects of gossypol on adult rat spermatogenic cells

J. Reyes, L. Borriero and D. J. Benos
Departamento de Fisiologia y Biofisica, Facultad de Medicina, Universidad de Chile, Santiago.

Rat spermatogenic cells have glycolytic rates of 124 +/- 36 nmol lactate.mg protein-1.h-1. Maximum glycolytic rates in the absence of oxidative phosphorylation do not exceed the basal rates by greater than 40%. From the rates of oxygen consumption and lactate production it can be calculated that less than 8% of the total ATP produced by spermatogenic cells is provided by glycolysis. These properties of spermatogenic cells would render them highly susceptible to cytotoxicity due to the action of agents like gossypol that impair mitochondrial oxidative phosphorylation or to conditions that produce testicular hypoxia. The main effect of gossypol on spermatogenic cell energy metabolism is to uncouple mitochondrial oxidative phosphorylation. In the absence of glucose, this uncoupling action of gossypol would change the NAD+/NADH redox coupling and, consequently, could modify metabolic fluxes through the lactic dehydrogenase catalyzed reaction.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online