L -Carnitine Attenuates Cigarette Smoke-Induced Apoptosis,Cytotoxicity,and Oxidative Stress in Human Vena Cava Endothelial Cells

Abstract

Background:

Cigarette smoke is widely recognized as a cause of oxidative stress. There is substantial evidence indicating that it can cause changes in the structure of the endothelium, leading to an increase in reactive oxygen species (ROS). l-carnitine (LC) is a compound that facilitates the transport of fatty acids to mitochondria and contributes to energy production and cellular apoptosis. Hence, this study aimed to explore the protective properties of LC against the cytotoxic effects triggered by cigarette smoke.

Materials and Methods:

Human vena cava endothelial cells (HUVECs) were exposed to cigarette smoke extract (CSE) and different concentrations of LC (50, 100, and 200 mM). The cytotoxicity was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Assessment of oxidative stress status included measuring ROS formation, malondialdehyde (MDA) levels, and glutathione (GSH) levels. Additionally, apoptotic and necrotic cells were quantified using Annexin V-Propidium Iodide co-staining through flow cytometry.

Results:

Our results showed that the presence of 200 μM CSE resulted in a 50% reduction in cell viability. However, LC restored cell viability. There was a significant decrease in the levels of ROS (p = 0.007, p = 0.0002, and p < 0.0001) with 50, 100, and 200 mM LC, respectively, in comparison to the CSE group. At a concentration of 200 mM, LC significantly elevated the intracellular GSH levels to 144 ± 10.44 (p < 0.0001) and markedly reduced MDA levels to 19.38 ± 2.01 (p = 0.0034) in comparison to the CSE-treated group. Flow cytometric analysis revealed a significant increase in cell death treated with CSE.

Conclusion:

In summary, this study’s results indicate that LC may mitigate CSE-induced toxicity by suppressing oxidative stress and apoptotic pathways.