Journal of Nutrition & Food Sciences
Open Access

Abstract

Garlic Extract Triggers Cytotoxicity, DNA Damage, and Cell Cycle Arrest in Human Leukemic Cells via Oxidative Stress

Sylvianne Njiki*, Keara Johnson, Jennifer N. Sims, Ariane M. Chitoh, Clement G. Yedjou*, Felicite K. Noubissi, Barbara Graham and Paul B. Tchounwou*

Garlic (Allium sativum) is one of the oldest medicinal plants that has received great attention throughout ancient and modern history. It has been used for the prevention and treatment of a wide variety of ailments, including cancer, cardiovascular disease, and hepatic and microbial infections. Although garlic shows potential in the prevention and treatment of cancer and other diseases, little is known about its therapeutic mechanisms of action. Here, we hypothesized that Garlic Extract (GE) induces cytotoxicity, DNA damage, and cell cycle arrest in Human Leukemia (HL-60) cells through oxidative stress. To test our hypothesis, HL-60 cells were treated with different concentrations (2 mg/mL, 4 mg/mL, and 6 mg/mL) of GE for 24 hours. Cell viability and cell morphology were analyzed by MTT, trypan blue, and Acridine Orange and Propidium Iodide (AO/PI) assays, respectively. The extent of oxidative stress was measured by the lipid peroxidation and glutathione peroxidase assays. The degree of DNA damage was evaluated by single-cell gel electrophoresis. Cell cycle arrest was assessed by the Cellometer Vision. Data obtained from the MTT assay, trypan blue dye, and AO/PI dye assessment indicated that GE significantly reduced the number of live cells in a concentration-dependent manner, showing a gradual increase in the loss of viability in GE-treated cells. MTT assay results also revealed that GE inhibits the viability of HL-60 cells, resulting in an IC₅₀ of 4.72 mg/mL. Tests for oxidative stress indicated significant increases (p<0.05) in the production of Malondialdehyde (MDA) and activity of glutathione peroxidase in GE-treated cells compared to the control group. Data obtained from the comet assay indicated that GE causes DNA damage in HL-60 cells in a concentration-dependent manner. GE treatment modulated cell cycle progression in HL-60 cells, leading to an arrest at the G2/M phase. In summary, our current investigation underscores that GE effectively curbs cell proliferation, induces DNA damage, and enforces cell cycle arrest of HL-60 cells, with these primary effects associated with oxidative stress. These findings contribute to a deeper understanding of the potential therapeutic role of GE in combating acute promyelocytic leukemia and other health challenges.

Published Date: 2025-05-28; Received Date: 2025-04-28