Salidroside prevents cadmium chloride-induced DNA damage in human fetal lung fibroblasts

Background: Cadmium (Cd) is an environmental pollutant and a heavy metal known for its genotoxic effects, which can lead to Cancer and other related diseases. Preventing Cd-induced genotoxicity is crucial; however, there is limited research on this topic. Salidroside (SAL), a phenylpropanoid glycoside isolated from Rhodiola rosea L., is a popular medicinal compound with several health benefits. Nevertheless, its therapeutic effect on Cd-induced genotoxicity remains unexplored.

Methods: Human fetal lung fibroblasts were treated with 20 μM Cd²⁺ (CdCl₂) for 12 h and 5-20 μM SAL was used to test the anti-DNA damage effect. DNA damage was evaluated using γH2AX expression and the alkaline comet assay. Intracellular Reactive Oxygen Species (ROS) levels were measured using flow cytometry.

Results: Exposure to 20 μM Cd²⁺ for 12 h induced significant DNA damage in human fetal lung fibroblasts, and this effect was notably attenuated by SAL treatment. SAL treatment did not decrease ROS levels in cells treated with Cd²⁺.

Conclusion: SAL effectively prevented Cd²⁺-induced DNA damage in human fetal lung fibroblasts. However, the underlying mechanism requires further investigation.

Cadmium; DNA damage; Genotoxicity; Natural extract; Salidroside.