Recent studies demonstrated that one isoform of angiotensin-converting enzyme named testicular or germinal (tACE) is localized in postmeiotic male germ cells and is essential for fertilizing ability of spermatozoa. Hypertension in spontaneously hypertensive rats (SHR) is androgen-dependent and reduction in male gametes is reported in this experimental conditions. Expression of tACE was not studied under conditions of spontaneous hypertension. The aim of this work is to characterize immunoexpression of tACE in the testis of adult (16-week-old) SHR rats in relation to the changes in blood pressure and serum testosterone level. In 82% of adult SHR, the immunoexpression of tACE followed the normal stage-specific pattern. Destructive testicular changes, germ cells depletion have been observed in 18% of 16-week-old SHR and stronger expression of tACE in stages 8-11compared to controls was detected. As a result stage specificity in SHR was not as evident as in control. No reaction was found in germ cell depleted tubules in which elongated spermatids were absent. Degenerating germ cells exhibited strong immunostaining comparable to that in residual bodies. The blood pressure was significantly higher in SHR and testosterone levels were more than twice but non-significantly elevated. There was no clear correlation between testicular structural changes, blood pressure level values or serum testosterone levels. Expression of tACE in postmeiotic germ cells, specifically altered by SHR, suggested possible involvement of components of reninangiotensin system in the process of spermiogenesis. Loss of enzyme expression we found in germ cell depleted tubules in SHR is due to absence of corresponding stages of spermatid differentiartion. Therefore, tACE can be used as a marker for germ cell depletion due to hypertension and other pathological conditions.

AbstractWe studied the effect of melatonin on morphological and functional disorders using serum markers of liver dysfunction such as cholinesterase and gamma glutamyl transpeptidase, hepatic protein content and malondialdehyde in a burned-rat model. Melatonin (10 mg/kg (−1), i.p) was administered immediately and then 12 h after 30% of total body surface area burns of male Wistar rats. The burns induced an increase of hepatic malondialdehyde levels by 166% (p<0.001), and also vascular congestion, leukocyte infiltration around the central veins, intracellular vacuolization, hepatic cell degeneration and apoptotic bodies (Councilman’s bodies). These changes were associated with significantly reduced serum cholinesterase (36%), gamma glutamyl transpeptidase (76%), hepatic proteins (52%) and serum albumin (37%) (p<0.001–0.0001). Treatment with melatonin reduced elevated hepatic malondialdehyde values by 50% (p<0.01). Melatonin restricted degenerative alteration in the hepatocytes: it protected the burninduced decrease of serum gamma glutamyl transpeptidase activity by 48% (p<0.01), hepatic proteins by 64% (p<0.01), and serum activity of cholinesterase as the only marker of liver damaged synthetic function by 57% (p<0.0001) but did not exert any significant influence on serum albumin concentration. Melatonin repaired the pathomorphological lesions and functional disorders. It could restore liver damage following thermal injury in humans.