Functional and histopathological kidney injury in hyperandrogenic female rats - a polycystic ovary animal model

Abstract

Background. Polycystic ovary syndrome (PCOS) is the most common reproductive disorder in premenopausal women. This syndrome is also associated with many metabolic and cardiovascular complications. These complications are major risk factors for renal injury and kidney disease. Therefore, this study aimed to investigate the types of functional and structural kidney injuries in a hyperandrogenic female rat model. Methods. Female Sprague-Dawley rats were randomly divided into three groups (n=10 each): control, sham, and dehydroepiandrosterone (DHEA). Plasma total testosterone and kidney functional indices were measured using enzyme-linked immunosorbent assay (ELISA) and colorimetric techniques. Ovarian and renal histological changes were also evaluated qualitatively and quantitatively by Hematoxylin-Eosin (H&E) staining. Results. Plasma total testosterone in the DHEA group increased about 9-fold compared to the control and sham groups. There was also a significant increase in Cr, BUN, and absolute excretion of sodium ion. Insignificant increases in glomerular filtration rate (GFR), urine flow rate (V0), and absolute excretion of potassium ion were observed in DHEA group compared to other groups. However, significant damages were observed in the glomerular and tubular parts of the kidneys and the follicular parts of the ovaries in DHEA-receiving rats. Conclusion. Hyperandrogenemia is likely to cause systemic abnormalities through a variety of mechanisms, followed by obvious destruction of kidney and ovarian tissues. Accordingly, DHEA administration provides a useful animal model for studying the mechanism of PCOS-mediated renal injury. Practical Implications. The present study Findings can be helpful in identifying the mechanism of PCOS-induced renal injury, especially in younger women.

Differential Expression of Prophetic Variables of Diagnostic Importance Having Potential Role in the Development of Diabetic Nephropathy

“…End-stage renal illness is frequently more challenging to treat than other kidney diseases due to its complicated metabolic abnormalities 11,12 . In order to delay diabetic nephropathy, prompt prophylaxis and treatment are therefore crucial 20,21 . The role of mitochondrial damage caused by oxidative stress in diabetic nephropathy was investigated in this study.…”

“…In this investigation, a considerable drop in GSH concentration was discovered in the patient group, which may be related to the excessive formation of reactive oxygen species that results in the conversion of reduced form to oxidized form (GSSH) 13 . Superoxide dismutase is catalyzed by sodium oxide dismutase (SOD) to hydrogen peroxide (H2O2), which is then further reduced by glutathione peroxidase and catalase activity 21,24,25 . According to the current study, patients' SOD activity has significantly decreased when compared to controls 15 .…”

“…Because the number of antioxidant enzymes in extracellular fluids is typically very low, plasma proteins are more likely to be oxidized by ROS. As a result, higher levels of advanced oxidation protein products (AOPPs), also known as oxidized protein products, are frequently found in the plasma of dialysis patients 20,21,22 . The most prevalent plasma protein, albumin, was found to be the principal source of AOPPs in the plasma 25,26 .…”

“…The levels of superoxide dismutase (SOD) were measured 20 . Catalase was measured by the method through spectrophotometer 21 . GSH concentrations were measured by the method.…”

“…GSH concentrations were measured by the method. 19,21 The level of glutathione peroxidase (GPx) was measured by the method of Mills 22 . The levels of glutathione reductase were measured by the procedure 25 .…”