AIMTo determine the biochemical effect of di-(2-ethylhexyl) phthalate (DEHP) on testes, liver, kidneys and pancreas on day 10 in the process of degeneration of the seminiferous epithelium.

METHODSDiets containing 2% DEHP were given to male Crlj:CD1(ICR) mice for 10 days. The dose of DEHP was 0.90 +/- 0.52 mg/mouse/day. Their testes, livers, kidneys and pancreata were examined for detection of mono-(2-ethylhexyl) phthalate (MEHP), nitrogen oxides (NOx) produced by peroxidation of nitric oxide (NO) with free radicals, and lipid peroxidation induced by the chain reaction of free radicals.

RESULTSHistological observation and serum analysis showed the presence of severe spermatogenic disturbance, Leydig cell dysfunction, liver dysfunction and dehydration. Unexpectedly, the concentration of MEHP in the testes was extremely low compared with that in the liver. However, the concentration of the NOx in the testes was as high as the hepatic concentration. Furthermore, free radical-induced lipid peroxidation was histochemically detected in the testes but not in the liver.

CONCLUSIONThe results indicate that DEHP-induced aspermatogenesis is caused by the high sensitivity of the testicular tissues to MEHP rather than the specific accumulation or uptake of circulating MEHP into the testes.

Animals ; Body Weight ; drug effects ; Copper ; metabolism ; Diethylhexyl Phthalate ; analogs & derivatives ; metabolism ; pharmacology ; Iron ; metabolism ; Kidney ; drug effects ; metabolism ; Lipid Peroxidation ; drug effects ; Liver ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred ICR ; Nitrogen Oxides ; metabolism ; Pancreas ; drug effects ; metabolism ; Spermatogenesis ; drug effects ; Testis ; drug effects ; metabolism ; Testosterone ; blood ; Zinc ; metabolism

AIMTo report two cases of the left testicular artery arching over the left renal vein (LRV) before running downward to the testis.

METHODSThe subjects were obtained from two Japanese cadavers. During the student course of gross-anatomical dissection, the anatomical relationship between the testicular vessels and the renal vein was specifically observed.

RESULTSThe arching left testicular artery arose from the aorta below the LRV and made a loop around the LRV, which appeared to be mildly compressed between the arching artery and the psoas major muscle.

CONCLUSIONClinically, compression of the LRV between the abdominal aorta and the superior mesenteric artery occasionally induces LRV hypertension, resulting in varicocele, orthostatic proteinuria and hematuria. Considering that the incidence of a left arching testicular artery is higher than that of a right one, an arching left artery could be an additional cause of LRV hypertension.

Aged, 80 and over ; Arteries ; abnormalities ; Constriction, Pathologic ; complications ; Humans ; Hypertension ; etiology ; Male ; Renal Veins ; pathology ; Testis ; blood supply