<p>Glycine supplementation mitigates lead-induced renal injury in mice</p>

Abstract

Purpose: Lead (Pb) is an environmental pollutant responsible for various organ damages including renal injury. It seems that OS and associated events are crucial mechanisms of lead-induced renal dysfunction. The current study aimed to explore the potential protective effects of glycine against renal injury caused by lead in mice. Materials and methods: Mature male mice (n=32) were allocated into four groups. The following treatment regimens were the control (vehicle-treated); Pb-acetate (20 mg/kg/day, gavage); Pb-acetate + glycine (500 mg/kg/day, IP); and Pb-acetate + glycine (1,000 mg/kg/day, IP). Pb-acetate + glycine was administered for 14 consecutive days, Pb-acetate was given first and then glycine at least 6 hours later. On day 15, the subjects were anesthetized, and samples were collected. Serum biomarkers such as BUN and serum creatinine were monitored along with formation of reactive oxygen species, lipid peroxidation, kidney GSH level, and histopathological changes. Results: Based on the results, BUN and serum creatinine levels significantly increased ­following exposure to lead. Glycine supplementation (500 and 1,000 mg/kg, IP) decreased BUN and ­creatinine serum levels ( P <0.001). Biomarkers of OS were also reduced in renal tissue ­following glycine therapy in Pb-exposed mice ( P <0.001). Histopathological changes were observed in mice treated with lead as tubular dilation, protein cast, vacuolization, and inflammation. In this regard, glycine inhibited histopathological alterations in kidney caused by lead exposure. Conclusion: It was found that glycine treatment significantly mitigated Pb-induced renal injury most likely through alleviating OS and the associated deleterious outcomes on the kidney tissue. Keywords: amino acids, glycine, lead, heavy metals, oxidative stress, nephrotoxicity