Conclusion: The urease positive probiotic L. plantarum AD3 strain have the antioxidative and antiuremic efficacy in acetaminophen induced experimental rats.
A B S T R A C TAcetaminophen is a commonly used analgesic and antipyretic drug, high doses of which cause hepatic and renal injury. In development and progression of kidney disease research, it is necessary to have a suitable common drug to induce uremia and renal failure of rats. It is also required to select the threshold doses for the said drug; a therapeutic dose and toxic dose for kidney failure using standard guidelines. An acute toxicity of acetaminophen was conducted by the limit test at a dose of 2000 mg kgG 1 b.wt., on either sex rats (n = 5) and a main test was conducted by a dose progression factor of 3.2 times as per Organization of Economic Co-Operation and Development guidelines 425. Eighteen male albino rats (n = 18) were divided into three groups, group I served as control, groups II and III rats were administered 175 mg and 550 mg kgG 1 b.wt., acetaminophen intraperitoneally for 14 days, respectively. Different parameters were considered to analyze renal failure. Urea, creatinine, GOT, GPT and MDA levels were increased significantly (p<0.05) in group III, compared to groups I and II. Antioxidant enzymes like SOD, catalase and GSH level were decreased significantly (p<0.05) in group III rats, compared to group I and II rats. Increase in blood uremia profile indicated that the higher dose of acetaminophen causes uremia. Increase in the toxicity markers and lipid peroxidation marker enzymes indicate the nephrotoxicity. Histological structures of kidney of group III animals showed a severe disorganization of glomerulus and dilation of renal tubules. These results indicate that intraperitoneal injection of acetaminophen at high dose causes nephrotoxicity and renal cellular damage to experimental rats.
Oxygen is very important to the existence of life. Oxygen deficiency, defined as hypoxia, elicits adaptive responses in cells and tissues. Lower oxygen concentration can cause the alteration of renal function, affects the maintenance of a balance of the body fluids, electrolytes, pH, and blood pressure homeostasis. Impaired fluid regulation could, in addition, contribute to the precipitation of pulmonary edema and exacerbate hypoxemia which may accelerate the progression of chronic kidney disease. In this context, the present study attempted to evaluate the association of renal injury and oxidative stress at different atmospheric pressures (1829, 3657, and 5486 m). Limited fecal analysis of experimental animals was also done to evaluate the impact of hypobaric hypoxia on the composition of dominant gastrointestinal microbiota. The study was performed on 24 male Wister strain rats and divided into four groups (C, HA-I, HA-II, and HA-III), and exposure was carried out for seven days period. In hypoxic exposure rats, plasma urea, creatinine, electrolytes and malonaldehyde level elevated and catalase and superoxide dismutase level diminished significantly compared to the controls. Increase in blood uremia profile, toxicity markers, and lipid peroxidation marker enzymes indicated that hypoxia causes renal failure. Histological structures of the kidney of group HA-II and HA-III animals showed severe disorganization of glomerulus and dilation of renal tubules. These results indicate nephrotoxicity or acute renal failure can occur at hypobaric hypoxia and it also affected the gut microbial population. This alteration was observed significantly above 3000 m.
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