Protective Effects of Purple Waxy Corn on Aflatoxin B1-induced Oxidative Stress and Micronucleus in HepG2 Cells

Abstract

The purpose of this study was to investigate the protective effects of purple waxy corn extract (Zea may L.) on aflatoxin B1-induced cytotoxicity, oxidative stress and micronuclei in HepG2 cells. Purple waxy corn extract contained phenolics (187.15-341.65 µg gallic acid/mg), flavonoids (0.55-21.35 µg quercetin/ mg) and anthocyanins (43.70-220.43 mg cyanidin-3-glucoside/l). Antioxidant activities of the extracts were measured using oxygen radical absorbance capacity (1410.70-2214.49 µM trolox/mg) and ferric reducing/ antioxidant power (292.38-612.38 µM trolox/mg) assays. There were significant correlations between phenolic, flavonoid and anthocyanin content and antioxidant activities (R=0.740-0.778) of purple waxy corn extract. Studies in HepG2 cells found that 0.5 and 1 mg/ml purple waxy corn extract increased cell viability in AFB1-treated HepG2 cells. Purple waxy corn extract reduced intracellular ROS production, increased GSH content and antioxidant enzyme GR, GPx and GST activities and micronucleus in aflatoxin B1-treated HepG2 cells. Therefore, purple waxy corn extract reduced aflatoxin B1 toxicity through induction of antioxidant activities and, thus, inhibited oxidative stress-induced DNA damage caused by aflatoxin B1s.

Purple Waxy Corn Modifies the Expression of CYP3A4, N-acetyltransferase 2, and UGT1A6 in HepG2 and Caco-2 Cells

“…There was no significant difference in cell viability among the tested purple waxy corn concentrations (125 to 1,000 µg/mL), which is consistent with a previous study that reported that purple waxy corn at 3,000 µg/mL reduced Hep G2 cell viability to 60%. 23 Hence, the study continued using these concentrations. For ROS analysis, the DCFH-DA method was employed based on the reaction of ROS with DCFH-DA to create highly fluorescent dichlorofluorescein.…”

Elucidating the combined toxicity of aflatoxin B1 and fumonisin B1 on HepG2 cells based on respirometry and transcriptome analyses

“…Such toxicity could be induced by the loss of mitochondrial function creating a mitochondrial metabolic gridlock, such as the inhibition of mitochondrial respiration (Prakash et al 2022). The in vitro hepatotoxicity of AFB1 and FB1 has been reported in many studies using the HepG2 cells as the preferred liver model (Abdul and Chuturgoon 2021; Chen et al 2022; Singto et al 2020). Oxidative stress, inflammation, and mitochondrial dysfunction by targeting ROS, DNA, p53, and other signaling pathways have been documented as toxic mechanism of AFB1 (Li et al 2022).…”