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

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...

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Veröffentlicht in:Ecotoxicology (London) 2021-12, Vol.30 (10), p.2011-2023
Hauptverfasser: Wang, Jinhua, Deng, Wanfei, Zou, Ting, Bai, Binbin, Chang, Alan K, Ying, Xueping
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container_issue 10
container_start_page 2011
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creator Wang, Jinhua
Deng, Wanfei
Zou, Ting
Bai, Binbin
Chang, Alan K
Ying, Xueping
description 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 Cd 2+ 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. Significant increases in the levels of malondialdehyde (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.
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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 Cd 2+ 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. Significant increases in the levels of malondialdehyde (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. 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Significant increases in the levels of malondialdehyde (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. 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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 Cd 2+ 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. Significant increases in the levels of malondialdehyde (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.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s10646-021-02465-8</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record>
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subjects Amine oxidase (flavin-containing)
Anions
Apoptosis
Artificial seawater
Cadmium
Caspase-3
Clams
Cytochromes
Cytoplasmic organelles
Earth and Environmental Science
Ecology
Ecotoxicology
Environment
Environmental Management
Gills
Heavy metals
Hydrogen peroxide
Malate dehydrogenase
Malondialdehyde
Marine environment
Marine pollution
Membrane potential
Meretrix meretrix
Mitochondria
Monoamine oxidase
Organelles
Oxidase
Oxidative stress
Pollutants
Scavenging
Sea-water
Seawater
Superoxide
Superoxide anions
Toxicity
title Cadmium-induced oxidative stress in Meretrix meretrix gills leads to mitochondria-mediated apoptosis
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