Abstract
Calcium ion (Ca2+) is one of the key intracellular signals, which is implicated in the regulation of cell functions such as impregnation, cell proliferation, differentiation and death. Cadmium (Cd) is a toxic environmental pollutant that can disturb cell functions and even lead to cell death. Recently, we have found that Cd induced apoptosis in gill cells of the freshwater crab Sinopotamon henanense via caspase activation. In the present study, we further investigated the role of calcium signaling in the Cd-induced apoptosis in the animals. Our data showed that Cd triggered gill cell apoptosis which is evidenced by apoptotic DNA fragmentation, activations of caspases-3, -8 and -9 and the presence of apoptotic morphological features. Moreover, Cd elevated the intracellular concentration of Ca2+, the protein concentration of calmodulin (CaM) and the activity of Ca2+-ATPase in the gill cells of the crabs. Pretreatment of the animals with ethylene glycol-bis-(b-aminoethyl ether)-N,N,N’,N’-tetraacetic acid (EGTA), Ca2+ chelator, inhibited Cd-induced activation of caspases-3, -8 and -9 as well as blocked the Cd-triggered apoptotic DNA fragmentation. The apoptotic morphological features were no longer observed in gill cells pretreated with the Ca2+ signaling inhibitors before Cd treatment. Our results indicate that Cd evokes gill cell apoptosis through activating Ca2+-CaM signaling transduction pathway.
Highlights
Cadmium (Cd) is a non-essential toxic heavy metal widely spreaded in terrestrial and aquatic environments during mining and manufacturing
These results indicated that Cd is able to induce apoptosis in gill, which was consistent with our previous findings [10]
The second mechanism is the activation of DNA repair proteins such as heat shock proteins (HSP), protein disulfide isomerase (PDI) and DNA glycosylase [44,45,46]
Summary
Cadmium (Cd) is a non-essential toxic heavy metal widely spreaded in terrestrial and aquatic environments during mining and manufacturing. Cd accumulates in organisms by feeding and metabolic processes, whose toxicity is exemplified by an extremely long biological half-life within organisms (15–30 years), resulting in both acute and chronic toxicity. Acute exposure of animals to high dose of Cd can cause cell apoptosis within a short time [1,2], while longer term exposure to small amounts of Cd can result in tissue and organ damage and cell necrosis [3, 4]. Cells first swell and plasma membrane collapses and cells are rapidly lysed [5]. In the process of apoptosis, its membrane is intact [6]. Apoptosis is associated with morphological changes in the cell including cell shrinkage [7], deformation in the nucleus [8], chromatin condensation [9,10], DNA fragmentation [11] and formation of apoptotic bodies
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