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Texto completo SciELO Brasil
Cunha, F. Q
Costa, R. S
Coimbra, T. M
Texto completo
Id: lil-618052
Autor: Francescato, H. D. C; Chierice, J. R. A; Marin, E. C. S; Cunha, F. Q; Costa, R. S; Silva, C. G. A; Coimbra, T. M.
Título: Effect of endogenous hydrogen sulfide inhibition on structural and functional renal disturbances induced by gentamicin
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;45(3):244-249, Mar. 2012. ilus, tab.
Idioma: en.
Resumo: Animal models of gentamicin nephrotoxicity present acute tubular necrosis associated with inflammation, which can contribute to intensify the renal damage. Hydrogen sulfide (H2S) is a signaling molecule involved in inflammation. We evaluated the effect of DL-propargylglycine (PAG), an inhibitor of endogenous H2S formation, on the renal damage induced by gentamicin. Male Wistar rats (N = 8) were injected with 40 mg/kg gentamicin (im) twice a day for 9 days, some of them also received PAG (N = 8, 10 mg·kg-1·day-1, ip). Control rats (N = 6) were treated with saline or PAG only (N = 4). Twenty-four-hour urine samples were collected one day after the end of these treatments, blood samples were collected, the animals were sacrificed, and the kidneys were removed for quantification of H2S formation and histological and immunohistochemical studies. Gentamicin-treated rats presented higher sodium and potassium fractional excretion, increased plasma creatinine [4.06 (3.00; 5.87) mg percent] and urea levels, a greater number of macrophages/monocytes, and a higher score for tubular interstitial lesions [3.50 (3.00; 4.00)] in the renal cortex. These changes were associated with increased H2S formation in the kidneys from gentamicin-treated rats (230.60 ± 38.62 µg·mg protein-1·h-1) compared to control (21.12 ± 1.63) and PAG (11.44 ± 3.08). Treatment with PAG reduced this increase (171.60 ± 18.34), the disturbances in plasma creatinine levels [2.20 (1.92; 4.60) mg percent], macrophage infiltration, and score for tubular interstitial lesions [2.00 (2.00; 3.00)]. However, PAG did not interfere with the increase in fractional sodium excretion provoked by gentamicin. The protective effect of PAG on gentamicin nephrotoxicity was related, at least in part, to decreased H2S formation.
Descritores: Alquinos/farmacologia
Glicina/análogos & derivados
Sulfeto de Hidrogênio/antagonistas & inibidores
Necrose Tubular Aguda/induzido quimicamente
Sulfeto de Hidrogênio/metabolismo
Necrose Tubular Aguda/tratamento farmacológico
Ratos Wistar
Fatores de Tempo
Limites: Animais
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME

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