Mechanisms of Phytoremediation by Resveratrol against Cadmium Toxicity

Abstract

Cadmium (Cd) toxicity poses a significant threat to human health and the environment due to its widespread occurrence and persistence. In recent years, considerable attention has been directed towards exploring natural compounds with potential protective effects against Cd-induced toxicity. Among these compounds, resveratrol (RV) has emerged as a promising candidate, demonstrating a range of beneficial effects attributed to its antioxidant and anti-inflammatory properties. This literature review systematically evaluates the protective role of RV against Cd toxicity, considering the various mechanisms of action involved. A comprehensive analysis of both in vitro and in vivo studies is conducted to provide a comprehensive understanding of RV efficacy in mitigating Cd-induced damage. Additionally, this review highlights the importance of phytoremediation strategies in addressing Cd contamination, emphasizing the potential of RV in enhancing the efficiency of such remediation techniques. Through the integration of diverse research findings, this review underscores the therapeutic potential of RV in combating Cd toxicity and underscores the need for further investigation to elucidate its precise mechanisms of action and optimize its application in environmental and clinical settings.

Keywords: antioxidant; cadmium; intoxication; phytoremediation; resveratrol.

Figure 1

Structural formulas and sources of RV. This figure illustrates the structural formulas of cis-RV and trans-RV, two isomers of the polyphenolic compound RV. Additionally, it highlights various fruits which are known to be rich sources of RV. The cis and trans configurations refer to the spatial arrangement of the hydroxyl group (-OH) and hydrogen (H) attached to the carbon–carbon double bond in the RV molecule.

Figure 2

Molecular mechanisms of RV in reducing Cd toxicity at the cellular level. Cd can disrupt the oxidative/antioxidative status of cells, indirectly resulting in oxidative stress via weakening the antioxidative barrier by inducing ROS formation and increasing electron leakage from the mitochondrial respiratory chain, ultimately leading to mitophagy. The highly stressed cell state is also reflected in the ER, where inflammasome formation and activation occur due to the altered metabolic/enzymatic environment, eventually leading to pyroptosis. RV antioxidant action can revert stressful circumstances in both organelles by reducing ROS generation and counterbalancing the inflamed environment by activating antioxidant pathways and enhancing genes relevant to the cellular stress response via epigenetic modifications. At the molecular level, Cd action also activates various pathways, initiating defense responses and leading to apoptosis by over-activating EGFR and acting on multiple points of its signaling cascades. RV beneficial effects on the cell rely on activating specific effectors that exert their inhibitory potential directly on the most critical components of signaling cascades, effectively restoring phenotype by lowering the detrimental effects of their aberrant activation.