4.5 Article

Chemopreventive effect of riboflavin on the potassium bromate-induced renal toxicity in vivo

Journal

NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
Volume 393, Issue 12, Pages 2355-2364

Publisher

SPRINGER
DOI: 10.1007/s00210-020-01938-7

Keywords

Potassium bromate; Riboflavin; Kidney; Toxicity; Stress; Apoptosis

Funding

  1. King Saud University, Riyadh, Saudi Arabia [RSP-2020/225]

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Potassium bromate (PB) is a general food additive, flavor enhancer, a by-product of water disinfection, and a class 2 carcinogen. It exerts various toxic effects in a dose- and time-dependent manner in vivo. This study is to explore the chemopreventive efficacy of vitamin B-2(riboflavin, RF) in PB-administered Swiss albino rats. The rats were distributed into five groups: control (group 1), PB alone (group 2, 150 mg/kg), RF alone (group 3, 2 mg/kg), PB + RF1 (group 4, 150 and 2 mg/kg), and PB + RF2 (group 5, 150 and 4 mg/kg). All the rodents were sacrificed after the completion of the treatment cycle. Then, blood and kidney samples were subjected to biochemical analysis. Group 2 demonstrated vivid signs of renal toxicities evidenced by altered renal function markers (urea, creatinine, albumin, glutathione-S-transferase) and redox status parameters (superoxide dismutase, catalase, glutathione reductase, reduced glutathione, lipid, and protein oxidation products). However, group 3 exhibited a slight alteration in many of the parameters while groups 4 and 5 demonstrated dose-dependent chemopreventive efficiency of RF against PB-induced alterations. Besides, RF seemed to facilitate apoptosis as well as inhibition of the necrosis in the PB-pre-challenged groups, as demonstrated by the cleaved PARP and lactate dehydrogenase activity. Also, the histopathological analysis and comet assay validate the biochemical results of the treatment groups significantly. All these results plead that RF has a significant chemopreventive property against PB-induced toxicity in vivo. Therefore, RF is a suitable agent in preventing the PB-induced toxicities at the clinical and industrial levels.

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