Glycine Betaine Relieves Lead-Induced Hepatic and Renal Toxicity in Albino Rats

Farid Abdelrazek; Dawlat A Salama; Afaf Alharthi; Saeed A Asiri; Dina M Khodeer; Moath M Qarmush; Maysa A Mobasher; Mervat Ibrahim

doi:10.3390/toxics10050271

Glycine Betaine Relieves Lead-Induced Hepatic and Renal Toxicity in Albino Rats

Toxics. 2022 May 23;10(5):271. doi: 10.3390/toxics10050271.

Authors

Farid Abdelrazek¹, Dawlat A Salama¹, Afaf Alharthi², Saeed A Asiri³, Dina M Khodeer⁴, Moath M Qarmush⁵, Maysa A Mobasher⁶, Mervat Ibrahim¹

Affiliations

¹ Biochemistry Department, Faculty of Agriculture, Ain Shams University, Cairo 11566, Egypt.
² Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, Taif 21944, Saudi Arabia.
³ Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Najran University, Najran 61441, Saudi Arabia.
⁴ Department of Pharmacology & Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia 41522, Egypt.
⁵ Urology Department, Prince Sultan Military Medical City, Riyadh 12233, Saudi Arabia.
⁶ Department of Pathology, Biochemistry Division, College of Medicine, Jouf University, Sakaka 41412, Saudi Arabia.

Abstract

Lead (Pb) is a widespread and nondegradable environmental pollutant and affects several organs through oxidative mechanisms. This study was conducted to investigate the antioxidant protective effect of glycine betaine (GB) against Pb-induced renal and hepatic injury. Male albino rats (n = 45) were divided into three groups: G1 untreated control, G2 Pb-acetate (50 mg/kg/day), and G3 Pb-acetate (50 mg/kg/day) plus GB (250 mg/kg/day) administered for 6 weeks. For G3, Pb-acetate was administered first and followed by GB at least 4 h after. Pb-acetate treatment (G2) resulted in a significant decrease in renal function, including elevated creatinine and urea levels by 17.4% and 23.7%, respectively, and nonsignificant changes in serum uric acid levels. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphates (ALP) activities were significantly increased with Pb treatment by 37.6%, 59.3%, and 55.1%, respectively. Lipid peroxidation level was significantly increased by 7.8 times after 6 weeks of Pb-acetate treatment. The level of reduced glutathione (GSH-R) significantly declined after Pb-acetate treatment. Pb-acetate treatment also reduced the activities of superoxide dismutase (SOD), glutathione-S-transferase (GST), and glutathione peroxidase (GSH-PX) by 74.1%, 85.0%, and 40.8%, respectively. Treatment of Pb-intoxicated rats with GB resulted in a significant reduction in creatinine, urea, ALT, AST, and lipid peroxidation, as well as a significant increase in the level of GSH-R and in the activities of ALP, SOD, GST, and GSH-PX. The molecular interaction between GB and GSH-PX indicated that the activation of GSH-PX in Pb-intoxicated rats was not the result of GB binding to the catalytic site of GSH-PX. The affinity of GB to bind to the catalytic site of GSH-PX is lower than that of H₂O₂. Thus, GB significantly mitigates Pb-induced renal and liver injury through the activation of antioxidant enzymes and the prevention of Pb-induced oxidative damage in the kidney and liver.

Keywords: antioxidant enzymes; glycine betaine; kidney function; lead; lipid peroxidation; liver function; reduced glutathione.

Grants and funding

This research received no external funding.