Rapid and permanent lipid changes with death of testicular cells induced by exposure to cadmium

ZANETTI SR; AVELDAÑO MI

Villa Carlos Paz, Córdoba

Congreso; XLIV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2008

sociedad Argentina de Investigación en Bioquímica y Biología Molecular

RAPID AND PERMANENT LIPID CHANGES AFTER DEATH OF TESTICULAR CELLS INDUCED BY EXPOSURE TO CADMIUM Zanetti SR  and Aveldaño MI INIBIBB, CONICET-UNS, Bahía Blanca, Argentina E-mail: szanettii@criba.edu.ar   Because it selectively damages testicular capillary endothelial cells, exposure to cadmium results in hemorrhagic ischemia and hemato-testicular barrier disruption. Tight junctions between Sertoli cells are disassembled, followed by sloughing of dead Sertoli and germ cells to seminiferous tubule lumena. Here we studied the early and late effects of CdCl2 on rat testicular lipids. The early effects were similar to those of ischemia induced by testicular artery ligation. Two days after a single CdCl2 dose, visible hemorrhage and inflammatory edema was accompanied by a massive hydrolysis of germ cell 22:5-rich glycerophospholipids (GPL) (to free fatty acids and diacylglycerols), and of sphingomyelins (SM) containing normal and hydroxylated  polyenoic fatty acids (to the corresponding ceramides, Cer). Thirty and 45 days later, the testicular weight was reduced to less than one third and most of the original 22:5-GPL and their products had been removed from the testis. Cholesterol esters and triglycerides mirrored the GPL changes, suggesting they were formed as GPL fatty acids were eliminated, probably by phagocytes. By contrast, the Cer initially produced remained high and unchanged in the tissue. Whether this is due to physical seclusion of Cer in a space inaccessible to phagocytes or to a Cd-related inhibition of ceramidase remains to be established.