POSSIBLE ROLE OF SODIUM CROMOGLYCATE, A MAST CELL STABILIZER IN HALTING GENTAMICIN NEPHROTOXICITY IN RATS.
Keywords:
Gentamicin, Nephrotoxicity, Mast cellsAbstract
Gentamicin is commonly used in treating life threatening gram-negative bacterial infections, butmajor limitation is its
nephrotoxic effect. Free radical generation and reduction in antioxidantdefense mechanisms are mainly considered to be
involved in gentamicin induced nephrotoxicity,but the exact mechanism still remains unclear. Mast cells are infiltrated in the
inflamed kidneyand their degranulation releases various inflammatory mediators during various renal diseases.We have
investigated the possible involvement of mast cell stabilizer sodium cromoglycate[SCG] in halting gentamicinnephrotoxicity
in rats. Administration of gentamicin [GM] 100mg/kg i.p. for 10 days in rats induced nephrotoxicity,
characterized by significantly [P<0.05]increased serum creatinine, blood urea nitrogen, urinary protein, renal oxidative
stress and mastcell density, decreased creatinine clearance and histopathological alterations. Co-administrationof SCG
[24mg/kg/day] attenuated significantly [P<0.05], all these biochemical parameters,reduced mast cell density and prevented
the histological alteration such as intracellular edema,glomerulus narrowing and necrosis in epithelial cells of the proximal
tubules. It is concluded thatmast cells have a detrimental role in gentamicin-induced nephrotoxicity and SCG stabilizes
mastcells, reduces the release of various proinflammatory cytokines and thus, prevents the toxiceffects of GM as seen in
both, the biochemical and histopathological parameters.
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