Cadmium-induced oxidative stress in Meretrix meretrix gills leads to mitochondria-mediated apoptosis

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 target cell organelles of Cd toxicity. In this study, we investigated the effect of Cd on the mitochondria of Meretrix meretrix gill cells and the underlying mechanism of mitochondria-mediated apoptosis following exposure to the metal.Exposure of the clams to 1.5, 3, 6 and 12 mg L −1 Cd 2+ solutions led to swollen mitochondria compared with the untreated clams. The mitochondria also became vacuolated at the higher Cd 2+ concentrations.Biochemical assays showed that monoamine oxidase (MAO) activity and mitochondrial membrane potential (Δψm) increased at 1.5 mg L −1 Cd 2+ , but decreased at higher Cd 2+ 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 Cd 2+ concentrations. Signi cant increases in the levels of MDA and H 2 O 2 as well as in the activity levels of caspase-3, -8, and -9 were also observed in the Cd 2+ -treated clams. The results implied that Cd might induce apoptosis in M. meretrix via the mitochondrial caspase-dependent pathway.

Cadmium Highlights Common and Specific Responses of Two Freshwater Sentinel Species, Dreissena polymorpha and Dreissena rostriformis bugensis

“…In case of mitochondrial stress, HSPD1 protects proteins from misfolding and promotes the proper refolding of the unfolded peptides produced during stress [ 45 ]. The induction of a mitochondrial HSP response is consistent with the fact that mitochondria are known targets of cadmium [ 32 , 45 , 46 , 47 , 48 ].…”

“…Examining the subcellular localisation of the identified DAPs reveals a noteworthy proportion located in the mitochondria. Cadmium is a well-documented mitochondrial toxin, accumulating within these organelles in vertebrate and invertebrate organisms, including bivalves [ 45 , 46 , 47 , 48 ]. This accumulation results in mitochondrial uncoupling, impaired ATP synthesis, and cellular energy imbalance [ 69 , 70 , 71 ].…”

“…These observations imply more significant effects of cadmium on the QM gills, resulting in marked histological and physiological alterations. In gills of the clam, Meretrix meretrix , cadmium leads to mitochondria-mediated apoptosis with induction of caspases and disorganised ciliary orientation with impairment of microtubules [ 48 ]. Consistent with these protein alterations, changes in the proteasome are also specifically observed in QM.…”

“…Table S4: Gene Ontology Biological Process enrichment in zebra and quagga mussel gills after cadmium exposure. Table S5: Short Summary of protein functions extracts from online database annotations [ 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 …”

Quercetin alleviates cadmium-induced BRL-3A cell apoptosis by inhibiting oxidative stress and the PERK/IRE1α/ATF6 signaling pathway

“…Apoptosis, a cell autonomous death regulated by genes, is an important regulatory technique used for self-recovery after body injury. Apoptosis plays an important role in regulating the homeostasis of the body [35] . Through Hoechst 33342 staining (Figs.…”