Cadmium-induced mitochondrial dysfunction and oxidative damage in leaves of Solanum nigrum L

Cadmium (Cd) accumulation in Solanum nigrum L. is known to occur mainly in cell walls and vesicles. However, limited research has been conducted on the toxic effects of Cd specifically targeting mitochondria in S. nigrum leaves. This study aims to delineate the impact of Cd accumulation on mitochondrial structure and function in S. nigrum leaves, thereby providing a theoretical foundation for enhancing its application in phytoremediation of Cd-polluted soils. The results showed that the Cd content in mitochondria would gradually reach saturation with the increase of Cd treatment concentration. However, the accumulation of Cd led to osmotic pressure imbalance and morphological changes within mitochondria, which in turn caused a series of impairments in mitochondrial function. Cd severely damaged the energy metabolism function of mitochondria, especially under 200 microM CdCl₂ stress, the mitochondrial ATP content decreased by 90.65 % and the activity of H⁺-ATPase decreased by 80.65 %. Furthermore, reactive oxygen species (ROS) in mitochondria accumulated mainly in the form of H₂O₂. Compared with the non-Cd control group, the H₂O₂ content in the Cd-treated groups (50, 100, and 200 microM CdCl₂) increased by 61.62 %, 186.69 %, and 405.81 %, respectively. The inhibition of cellular respiration by Cd and the sharp increase in ROS exacerbated the oxidative damage in mitochondria. Interestingly, the activities of mitochondrial peroxidase (POD) and dehydroascorbate reductase (DHAR) exhibit remarkable tolerance under Cd stress. Based on these results, we believe that Cd can cause dysfunction and oxidative damage to the mitochondria of S. nigrum leaves.