Comparative study of piroxicam and nitroglycerin on prostaglandin-modulated blood and electrolyte indices during di-estrous in female Wistar Rats.

OBJECTIVE: Endogenous prostaglandins are involved in hemostasis, renal excretion of electrolytes, and implicated in dysmenorrhea. Piroxicam and Nitroglycerin are common drugs used in treating dysmenorrhea by inhibiting the cyclooxygenase pathway involved in prostaglandin production. However, studies comparing the effects of these drugs on prostaglandin-modulated hemostasis and renal function are lacking. METHODS: Fifteen female rats (120-160g) were divided into 3 groups (20 per group), namely Control (distilled water, 0.3 mL), Piroxicam treated (3mg/kg) and Nitroglycerin treated (1 mg/kg). Di-estrous phase was confirmed in animals in each group using the Pipette smear method. Treatment was administered for 4 days covering the estrous cycle. Bleeding and clotting time were assessed and blood concentrations of sodium, potassium, urea and platelet counts were evaluated in all phases. Data were analyzed using one-way ANOVA and Newman-Keuls post-hoc test. Statistical significance was considered at p<0.0. RESULTS: The nitroglycerin-treated group showed significant increases in blood potassium during di-estrous while the piroxicam-treated group showed significant increases in blood potassium, urea and clotting time with a significant decrease in sodium levels during di-estrous compared to controls. Results obtained in other phases were not significant compared to controls. CONCLUSIONS: The study showed that Nitroglycerin produces minimum alteration of blood and electrolyte indices compared to piroxicam during di-estrous.

Exposure to ultraviolet radiation during pregnancy influences offspring immune and inflammatory responses in Wistar-strain rats.

OBJECTIVE: During pregnancy, maternal exposure to ultraviolet radiation (UVR) has been linked to altered offspring immune and health status. This study was therefore designed to investigate some markers of immune response in the offspring of pregnant Wistar rats exposed to UVR at various points of gestation. METHODS: Thirty pregnant rats were divided into 6 groups (n=5) as follows; group I, control, consisting of pregnant rats unexposed to UVR. Animals in groups II, III, IV, V and VI were exposed to UVR for one hour daily, on gestational days 1-7,8-14,15-21,1-14 and 1-21, respectively. Animals were allowed to come to term and offspring birth weight was taken. On postnatal Day 10, weight of each offspring was taken again. Thereafter, blood samples were collected from each offspring per group and evaluated for total protein, albumin, globulin, C-reactive protein, interleukin-1ß, and complement component protein-3 (C3). Offspring hepatic samples were evaluated using standard histological techniques. RESULTS: Offspring birthweight increased (p<0.05), while weight gain on postnatal day 10 reduced in all experimental groups compared to controls. No significant differences were observed for offspring total protein, albumin, and C3 levels across all groups. Globulin increased (p<0.05) only in group VI, while C-reactive protein increased (p<0.05) in all experimental groups, except group III, compared to controls. Interleukin-1ß in groups II, III, V and VI increased significantly compared to controls. Offspring hepatic samples exhibited hepatocellular degeneration and necrosis that was independent of gestational stage of maternal exposure to UVR. CONCLUSIONS: Maternal exposure to ultraviolet radiation during gestation in Wistar rats activates offspring immune and inflammatory responses.

Selenium Supplementation Increases Hepatic Glucose-6-Phosphatase and Peroxisome Proliferator Activated Receptor Gamma Coactivator-1α Activity in Male Wistar Rats.

Increased selenium supplementation has been implicated in diabetes mellitus via peroxisome-proliferator-activated-receptor-gamma-coactivator-1-alpha (PGC-1α) associated pathways. This study was designed to investigate the effect of selenium supplementation on PGC-1α and glucose-6-phosphatase (G6Pase) as well its likely hepato toxicity in male Wistar rats. Animals were randomly divided into 3 groups (n=10/group) and treated orally with water (0.2ml - group 1) or selenium (25µg/day -group 2; 50µg/day - group 3) for 28 and 56days, respectively. Thereafter, blood samples were collected and estimated for glucose, alkaline-phosphate (ALP), gamma-glutamyltransferase (GGT) and aspartate-aminotransferase (AST). Liver homogenates were analyzed for PGC-1α and G6Pase activity. Significant dose-dependent increases in blood glucose, hepatic PGC-1α and G6Pase activities were observed on days 28 and 56 in selenium groups compared to group 1. Serum GGT activity increased in both selenium groups on day 28 however, on day 56 values in group 2 were reduced and increased in group 3, respectively. Compared to control ALP reduced in selenium groups while AST was not significantly different. This study suggests that selenium supplementation increases hepatic peroxisome-proliferator-activated-receptor-gamma-coactivator-1α and glucose-6-phosphatase activity leading to a likely increase in hepatic glucose output. It also shows that though selenium supplementation at the doses used maybe nontoxic to hepatocytes, it may however exert potential toxicity on the biliary tract.