Riboflavin potentially attenuates arsenic hepatotoxicity: a focus on oxidative changes, apoptosis, and PINK1 pathway

In natural ways and as a result of human activity arsenic (As2O3) is widely distributed in our surroundings, with toxic effects on liver functions. This study investigates riboflavin's hepatoprotection (a flavoproteins component) on toxicity induced by As2O3. Twenty-four male Wistar rats were randomly assigned into four equal groups, and the experimental group orally received As2O3 (3 mg/L/day) alone or in combination with riboflavin (40 mg/L/day) for 30 consecutive days. To detect liver abnormalities the major oxidative stress indices (reactive oxygen species and total antioxidative status), lipid peroxidation (malondialdehyde (MDA)), inflammatory markers (interleukin 6 and C-reactive protein), liver enzymes, and mRNA expression levels of apoptosis and PINK1 pathway genes (for mitochondrial quality control) were evaluated. p < 0.05 was considered statistically significant. After receiving As2O3, blood serum levels of oxidative stress indices, MDA production, inflammatory markers, and liver enzymes increased. Regarding the genes expression profile of apoptosis (Bax and TNF-ɑ) and PINK1 pathway (PINK1, Parkin, LC3-I, Mfn2, Fis1, and p38), As2O3 upregulated all expressions (except Bcl-2). Riboflavin therapy is potentially an effective strategy for modifying hepatic dysfunction via As2O3 damages through the abrogation of oxidative changes. These findings can enhance the clinical diagnosis of hepatotoxicity. © 2023, The Author(s), under exclusive licence to Springer-Verlag London Ltd., part of Springer Nature.