Abstract
Cadmium (Cd) is one of the most important marine environmental pollutants that can cause oxidative damage and apoptosis in living organisms, and mitochondria are the key cell organelles affected by Cd toxicity. In this study, we investigated the effect of Cd on the mitochondria in the gill cells of the clam Meretrix meretrix and the underlying mechanism of mitochondria-mediated apoptosis following exposure to the metal. Exposure of the clams to artificial seawater containing 1.5, 3, 6 and 12 mg L-1 Cd2+ led to swollen mitochondria compared with the untreated clams. The mitochondria also became vacuolated at the higher Cd2+ concentrations. Biochemical assays showed that monoamine oxidase (MAO) activity and mitochondrial membrane potential (Δψm) increased at 1.5 mg L-1 Cd2+, but decreased at higher Cd2+ concentrations, while the activities of malate dehydrogenase (MDH) and cytochrome oxidase (CCO) and the scavenging capacities of anti-superoxide anion (ASA) and anti-hydroxy radical (AHR) all decreased with increasing Cd2+ concentrations. Significant increases in the levels of malondialdehyde (MDA) and H2O2 as well as in the activity levels of caspase-3, -8, and -9 were also observed in the Cd2+-treated clams. The results implied that Cd might induce apoptosis in M. meretrix via the mitochondrial caspase-dependent pathway.
Highlights
In recent years, pollution caused by toxic metals has become a serious environmental problem that continues to increase in magnitude as a result of rapid industrialization and the massive use of fertilizers (Chen et al, 2020; Zhang and Gao, 2015)
Biochemical assays showed that monoamine oxidase (MAO) activity and mitochondrial membrane potential (Δψm) increased at 1.5 mg L−1 Cd2+, but decreased at higher Cd2+ concentrations, while the activities of malate dehydrogenase (MDH) and cytochrome oxidase (CCO) and the scavenging capacities of anti-superoxide anion (ASA) and anti-hydroxy radical (AHR) all decreased with increasing Cd2+ concentrations
The gills of bivalves are suitable for histopathological analysis since they consist of a simple epithelium with various cell types, in which the effects caused by toxic metals in the water can be observed (Trevisan et al, 2014; Zhen et al, 2018)
Summary
Pollution caused by toxic metals has become a serious environmental problem that continues to increase in magnitude as a result of rapid industrialization and the massive use of fertilizers (Chen et al, 2020; Zhang and Gao, 2015). Mitochondria are the key intracellular targets for Cd stress (Bhansali et al, 2017), and Cd exposure can damage the integrity of the mitochondria in aquatic organisms, both structurally and functionally (Adiele et al, 2011). Ji et al (2019) found that Cd can induce the reconstruction of energy homeostasis, stress resistance and apoptosis in Ruditapes philippinarum, and suggested that mitochondria are the key target of Cd toxicity in clams. Mitochondria are a major source of superoxide radical (O2−) and hydrogen peroxide (H2O2) in a cell (Bhansali et al, 2017), and Cd has been shown to facilitate the formation of reactive oxygen species (ROS) by interfering with the electron transport chain in the mitochondria, stimulating lipid peroxidation via the oxidation of polyunsaturated fatty acids in organisms such as the bivalves (Goswami et al, 2014; Ji et al, 2019)
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