N-acetylcysteine protects against star fruit-induced acute kidney injury

N-acetylcysteine protects against star fruit-induced acute kidney injury

Author Shimizu, Maria Heloisa Massola Google Scholar
Gois, Pedro Henrique Franca Google Scholar
Volpini, Rildo Aparecido Google Scholar
Canale, Daniele Google Scholar
Luchi, Weverton Machado Google Scholar
Froeder, Leila Autor UNIFESP Google Scholar
Heilberg, Ita Pfeferman Autor UNIFESP Google Scholar
Seguro, Antonio Carlos Google Scholar
Abstract Background: Star fruit (SF) is a popular fruit, commonly cultivated in many tropical countries, that contains large amount of oxalate. Acute oxalate nephropathy and direct renal tubular damage through release of free radicals are the main mechanisms involved in SF-induced acute kidney injury (AKI). The aim of this study was to evaluate the protective effect of N-acetylcysteine (NAC) on SF-induced nephrotoxicity due to its potent antioxidant effect. Materials and methods: Male Wistar rats received SF juice (4 mL/100 g body weight) by gavage after a 12 h fasting and water deprivation. Fasting and water deprivation continued for 6 h thereafter to warrant juice absorption. Thereafter, animals were allocated to three experimental groups: SF (n = 6): received tap water

SF+NAC (n = 6): received NAC (4.8 g/L) in drinking water for 48 h after gavage

and Sham (n = 6): no interventions. After 48 h, inulin clearance studies were performed to determine glomerular filtration rate. In a second series of experiment, rats were housed in metabolic cages for additional assessments. Results: SF rats showed markedly reduced inulin clearance associated with hyperoxaluria, renal tubular damage, increased oxidative stress and inflammation. NAC treatment ameliorated all these alterations. Under polarized light microscopy, SF rats exhibited intense calcium oxalate birefringence crystals deposition, dilation of renal tubules and tubular epithelial degeneration, which were attenuate by NAC therapy. Conclusions: Our data show that therapeutic NAC attenuates renal dysfunction in a model of acute oxalate nephropathy following SF ingestion by reducing oxidative stress, oxaluria, and inflammation. This might represent a novel indication of NAC for the treatment of SF-induced AKI.
Keywords Acute kidney injury
acute oxalate nephropathy
oxidative stress
star fruit
xmlui.dri2xhtml.METS-1.0.item-coverage Abingdon
Language English
Sponsor Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Grant number CNPq: 306148/2013-7
FAPESP: 2014/25567-6
FAPESP: 2015/11933-3
Date 2017
Published in Renal Failure. Abingdon, v. 39, n. 1, p. 193-202, 2017.
ISSN 0886-022X (Sherpa/Romeo, impact factor)
Publisher Taylor & Francis Ltd
Extent 193-202
Origin http://dx.doi.org/10.1080/0886022X.2016.1256315
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000394441100028
URI https://repositorio.unifesp.br/handle/11600/56404

Show full item record


File Size Format View

There are no files associated with this item.

This item appears in the following Collection(s)




My Account