Abstract
We studied here the short-term toxicity effects of Cd on the oxidative state and cell death in the gill of freshwater crab Sinopotamon henanense. Crabs were exposed to Cd that resulted in Cd accumulation and a significant increase in the metallothionein (MT) level in the gill, but MT level increased disproportionally compared to the Cd accumulation with an extension of exposure time. Significant changes in the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were observed. An increase in the levels of reactive oxygen species (ROS) and lipid peroxidation (LPO) was detected that will cause oxidative stress. Histological abnormalities of the gills were discovered, including the expansion of gill cavity, a decrease in the numbers of connection of the upper and the lower of the gill lamellae and epithelial cells, and an increase in the number of hemocytes. The results of a TUNEL test and transmission electron microscope (TEM) showed that more gill cells had apoptotic characteristics after 48 h of Cd treatment compared to the control, but epithelial cell necrosis and inflammatory response appeared only after 72 h. It was concluded that (1) Cd induced the ROS production and accumulation through inhibiting antioxidant enzyme activities and exceeding the saturation values of MT binging; (2) Cd led to lipid peroxidation and histopathological alternations; and (3) Cd induced apoptotic response at short time exposure, followed by necrotic features and inflammatory reaction after longer time exposure.
Highlights
Heavy metal pollution of the aquatic environment may be caused by natural and anthropogenic activities
We investigated short-term toxicity effects of acute Cd exposure on the oxidative state, histological structure and cell death in the gill
Cd concentration assay in water The Cd concentration in water from each treatment group was analyzed during the experiment
Summary
Heavy metal pollution of the aquatic environment may be caused by natural and anthropogenic activities. Cadmium (Cd), one of the toxic heavy metals, enters aquatic organisms by their food and from the ambient environment through gills and epithelia where it is taken up through calcium channels of the plasma membrane of cells [1]. One aspect of cadmium toxicities is the generation of cytotoxic reactive oxygen species (ROS) that cause oxidative deterioration of biological macromolecules [9]. There is a balance between ROS production and antioxidant defense which is an important removal mechanism of reactive oxygen species. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) constitute a part of the antioxidant system that protects cells against ROS. When the rate of ROS generation exceeds the antioxidant capacity of cells, severe oxidative stress will result in oxidative damage. In addition to the enzyme index, a central measure of oxidative stress is lipid peroxidation (LPO), as indicated by malondialdehyde (MDA) levels, which can accumulate as a consequence of cellular damage [10,11]
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