Protective effects of Dioscorea polystachya ethanol extracts against lead acetate-induced oxidative DNA damage in MRC-5 cells

• Published in: Molecular & cellular toxicology Vol. 18; no. 4; pp. 581 - 588
• Main Authors: Jeong, Seula, Chung, Yuheon, Moon, Jonghyun, Kim, Youngun, Kim, Seulhye, Baek, Gain, Park, Jong Kun
• Format: Journal Article
• Language: English
• Published: Singapore Springer Nature Singapore 01-10-2022; Springer Nature B.V; 대한독성 유전단백체 학회
• Subjects: Apoptosis; BAX protein; BIM protein; Biomedical and Life Sciences; Cell Biology; Cell viability; Deoxyribonucleic acid; Dioscorea polystachya; DNA; DNA damage; DNA fragmentation; Ethanol; Fossil fuels; Heavy metals; Herbal medicine; Inflammation; Lead; Life Sciences; Original Article; Oxidation; p53 Protein; Particulate matter; Pharmacology/Toxicology; Proteins; Reactive oxygen species; Respiratory diseases; Respiratory system; 생물학; Lead; DNA damage response; Particulate matter
• ISSN: 1738-642X; 2092-8467
• DOI: 10.1007/s13273-022-00230-4

Background
Lead (Pb), a heavy metal, is contained in large amounts of particulate matter (PM). The greater production of PM through agricultural operations, industrial processes, and combustion of fossil fuels concomitantly increases human exposure to lead through the respiratory system. Lead is highly toxic even when exposed in small amounts to the body and induces respiratory diseases, increased production of reactive oxygen species (ROS), and DNA damage.
Dioscorea polystachya
(DP) possesses antioxidant and anti-inflammatory effects and is used as a traditional herbal remedy to treat respiratory diseases. However, the effects of DP on oxidative DNA damage remain unclear.
Objective
In this study, we determined the protective effects of DP ethanol extracts (DEE) against the lead acetate-induced oxidative DNA damage in MRC-5 cells—a human lung fibroblast cell line.
Result
MRC-5 cells were co-treated with 200 μM of lead acetate and various concentrations of DEE for 48 h. Cell viability, which decreased by approximately 40% after treatment with lead acetate alone, showed an approximately 34% increase upon treatment with 500 μg/mL DEE. The increased levels of 8-OHdG, DNA fragmentation and cellular ROS observed upon treatment with lead acetate, decreased in a DEE concentration-dependent manner. Furthermore, the levels of DNA damage response (DDR)-related proteins, such as p53, p-p53, and p21 increased, and the levels of apoptosis-related proteins, such as Bax and Bim decreased in a DEE concentration-dependent manner.
Conclusion
Our results demonstrate the protective effects of DEE on lead acetate-induced oxidative DNA damage, mediated through a reduction in the levels of cellular ROS and an increase in those of DDR-related proteins at early time points.