Rapid And Permanent Lipid Changes After Death Of Testicular Cells Induced By Exposure To Cadmium

Abstract

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 lumen. Here we studied the early and late effects of CdCl on rat testicular lipids. 2 The early effects were similar to those of ischemia induced by testicular artery ligation. Two days after a single CdCl dose, visible 2 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