Abstract
It is said that a wide range of renal functions are at risk from arsenic exposure. We examined how lactoferrin administration may mitigate inflammation, apoptosis, redox imbalance, and fibrosis in order to counteract arsenic-induced nephrotoxicity. Accordingly, male C57BL/6 mice (6 weeks) were divided into six experimental groups with six mice in each group. The first and second groups were intragastrically administered normal saline and sodium arsenite (NaAsO2) at 5 mg/kg body weight concentrations as the negative control (NC) and NaAsO2 groups. The third, fourth, and fifth groups were intragastrically administered lactoferrin at concentrations of 100, 200, and 400 mg/kg body weight in addition to NaAsO2 at concentrations of 5 mg/kg body weight. The sixth group was intragastrically administered lactoferrin at a concentration of 200 mg/kg body weight with the experimental group set as the lactoferrin group. After daily drug administration for 4 weeks, the lactoferrin concentrations were optimized based on the results of renal index and renal function. Histopathological, biochemical, and gene expression analyses were performed to evaluate the status of renal tissue architecture, redox imbalance, inflammation, apoptosis, and fibrosis to confirm the alleviative effect of lactoferrin treatment against the NaAsO2 exposure-induced nephrotoxicity. The results confirmed that the 200 mg/kg lactoferrin treatment mitigated these arsenic effects and maintained the normal renal frameworks. Conclusively, disrupting the renal redox balance and triggering inflammation, apoptosis, along with fibrosis is a milieu that arsenic, robustly exerts its nephrotoxic effect. Lactoferrin, probably by its direct and indirect control mechanism on these said pathways, can mitigate the nephrotoxicity and preserve the normal renal health.