Introduction: Nephrotic syndrome induced by adriamycin (ADR) is an experimental model of glomerulosclerosis in humans. The AT 1 receptor for angiotensin II (Ang II) is involved in the renal expression of the nuclear factor-kappa B (NF-ΚB) during this nephrosis. NF-ΚB is a transcription factor for proinflammatory effects of Ang II; however, there is no information about the role of this receptor in the renal proinflammatory events in ADR nephrosis. Materials and methods:To determine the role of Ang II in ADR nephrosis, Sprague-Dawley rats were treated with ADR (6 mg/kg iv). One ADR group received oral losartan treatment (15 mg/kg gavage) 3 days before ADR injection and then daily for 4 weeks, and the other group water. Animals were sacrificed at week 4 and renal macrophage infiltration, ICAM-1, superoxide anion (O 2 -) and Ang II expressions were analysed by indirect immunofluorescence and histochemical techniques. Results: ADR rats showed increased expression of ICAM-1, Ang II, O 2 -and macrophage infiltration, events that were diminished by losartan treatment. Ang II expression remained unaltered after antagonist treatment. Proteinuria was reduced after 3 weeks of treatment. Conclusions: These data suggest that Ang II plays a role in the inflammatory events during ADR-induced nephrosis, probably mediated by AT 1 receptors.
Creatine kinase activity was measured in the seminal fluid of 70 males undergoing fertility studies. The average value obtained at 30°C was 333 f 197 IUil (average ? SD). There was no evidence of a significant correlation between creatine kinase enzymatic activity and density, active lineal motility, or number of normal motile spermatozoa; nor was there any correlation seen between creatine kinase activity and concentration of citric acid, (indicator of prostatic function) or fructose, (indicator of seminal vesicle function). Nonetheless, in two cases of excretory azoospermia, very high values of creatine kinase (2510 and 1280 IU/I) and citric acid levels (4000 and 3000 mg/dl) were observed. These would indicate that the origin of creatine kinase is fundamentally prostatic, in contradiction to previous studies by other authors. In this sense, creatine kinase would be a parameter of prostatic function in studies of male fertility. In two cases of secretory azoospermia due to cryptorchidism and in several very severe oligoasthenozoospermias, low creatine kinase levels were seen, while fructose and citric acid levels were normal. This would give relative value to creatine kinase as an indicator of spermatogenesis.
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