» Articles » PMID: 30632398

Effects of Alpha-lipoic Acid on High Fructose Induced Hepatic Pathology

Overview
Specialty Biochemistry
Date 2019 Jan 12
PMID 30632398
Citations 1
Authors
Affiliations
Soon will be listed here.
Abstract

Little is known about the pathogenesis of high fructose corn syrup (HFCS) induced hepatic toxicity. We investigated hepatic lesions induced by chronic HFCS consumption and the protective effects of alpha-lipoic acid (ALA) on liver pathology. We used 24 rats allocated randomly into three groups of eight. The HFCS group was given in drinking water for 10 weeks. The ALA + HFCS group was given the same dose of HFCS and ALA also was administered during the last 6 weeks of the experiment. The control group was untreated. The rats were euthanized at the end of 10 weeks and 24 h after the last ALA administration. A significant increase was observed in the serum aspartate aminotransferase (AST) level of the HFCS group compared to controls. Tissue malondialdehyde (MDA) levels also increased significantly and catalase (CAT) activity decreased significantly in the HFCS group. Caspase-3 expression increased significantly in the HFCS group compared to controls. In the ALA treated group, the levels of MDA, CAT and caspase-3 returned to near control levels. HFCS caused hepatic toxicity by increasing oxidative stress and apoptosis. ALA administration ameliorated the pathological changes.

Citing Articles

The Effect of Boric Acid on Oxidative Stress, Inflammation, and Apoptosis in Embryonic and Fetal Tissues Damage Caused by Consumption of High-Fructose Corn Syrup in Pregnant Rats.

Basegmez M, Yuksel D Reprod Sci. 2025; 32(2):514-525.

PMID: 39821796 PMC: 11825574. DOI: 10.1007/s43032-025-01792-z.


The protective role of selenium against high-fructose corn syrup-induced kidney damage: a histopathological and molecular analysis.

Tepebasi M, Savran M, Cosan S, Tastan S, Aydin B Naunyn Schmiedebergs Arch Pharmacol. 2024; 397(10):7829-7837.

PMID: 38734838 PMC: 11450133. DOI: 10.1007/s00210-024-03149-w.