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Glycine supplementation mitigates lead-induced renal injury in mice
Mojtaba Shafiekhani1,2, Mohammad Mehdi Ommati3, Negar Azarpira4
1Toxin Research Center, Faculty of Medicine, Aja University of Medical Science, Tehran, Iran, Amir.salarian@ajaums.ac.ir.
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.
Insights
Glycine supplementation effectively protected mice against lead-induced kidney damage by reducing oxidative stress and improving renal function markers. This study highlights glycine
Area of Science:
- Environmental toxicology
- Nephrology
- Biochemistry
Background:
- Lead (Pb) is a pervasive environmental pollutant known to cause significant organ damage, particularly renal injury.
- Oxidative stress (OS) and its related mechanisms are implicated as key contributors to lead-induced renal dysfunction.
Purpose of the Study:
- To investigate the potential protective effects of glycine against lead-induced renal injury in a mouse model.
- To evaluate glycine's impact on oxidative stress markers and renal function following lead exposure.
Main Methods:
- Male mice were divided into four groups: control, lead acetate exposure, and lead acetate with two different doses of glycine.
- Mice received treatments for 14 days, with serum biomarkers (BUN, creatinine), oxidative stress markers (ROS, lipid peroxidation, GSH), and kidney histopathology assessed.
Main Results:
- Lead exposure significantly elevated blood urea nitrogen (BUN) and serum creatinine levels, indicating renal dysfunction.
- Glycine supplementation at both 500 and 1,000 mg/kg doses significantly reduced BUN and creatinine levels (P<0.001).
- Glycine treatment also decreased biomarkers of oxidative stress and mitigated lead-induced histopathological changes in kidney tissue, including tubular dilation and inflammation.
Conclusions:
- Glycine treatment significantly ameliorated lead-induced renal injury in mice.
- The protective effects of glycine are likely mediated by its ability to alleviate oxidative stress and its downstream consequences on kidney tissue.
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