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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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. |
doi_str_mv | 10.1007/s10646-021-02465-8 |
format | Article |
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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.</description><identifier>ISSN: 0963-9292</identifier><identifier>EISSN: 1573-3017</identifier><identifier>DOI: 10.1007/s10646-021-02465-8</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>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</subject><ispartof>Ecotoxicology (London), 2021-12, Vol.30 (10), p.2011-2023</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>COPYRIGHT 2021 Springer</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-37611a8d51d355d17a382c6a3d06dcc08c7d9ce251b4375e566ee1de650b67a73</citedby><cites>FETCH-LOGICAL-c463t-37611a8d51d355d17a382c6a3d06dcc08c7d9ce251b4375e566ee1de650b67a73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10646-021-02465-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10646-021-02465-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids></links><search><creatorcontrib>Wang, Jinhua</creatorcontrib><creatorcontrib>Deng, Wanfei</creatorcontrib><creatorcontrib>Zou, Ting</creatorcontrib><creatorcontrib>Bai, Binbin</creatorcontrib><creatorcontrib>Chang, Alan K</creatorcontrib><creatorcontrib>Ying, Xueping</creatorcontrib><title>Cadmium-induced oxidative stress in Meretrix meretrix gills leads to mitochondria-mediated apoptosis</title><title>Ecotoxicology (London)</title><addtitle>Ecotoxicology</addtitle><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.</description><subject>Amine oxidase (flavin-containing)</subject><subject>Anions</subject><subject>Apoptosis</subject><subject>Artificial seawater</subject><subject>Cadmium</subject><subject>Caspase-3</subject><subject>Clams</subject><subject>Cytochromes</subject><subject>Cytoplasmic organelles</subject><subject>Earth and Environmental Science</subject><subject>Ecology</subject><subject>Ecotoxicology</subject><subject>Environment</subject><subject>Environmental Management</subject><subject>Gills</subject><subject>Heavy metals</subject><subject>Hydrogen peroxide</subject><subject>Malate dehydrogenase</subject><subject>Malondialdehyde</subject><subject>Marine environment</subject><subject>Marine pollution</subject><subject>Membrane potential</subject><subject>Meretrix meretrix</subject><subject>Mitochondria</subject><subject>Monoamine oxidase</subject><subject>Organelles</subject><subject>Oxidase</subject><subject>Oxidative stress</subject><subject>Pollutants</subject><subject>Scavenging</subject><subject>Sea-water</subject><subject>Seawater</subject><subject>Superoxide</subject><subject>Superoxide anions</subject><subject>Toxicity</subject><issn>0963-9292</issn><issn>1573-3017</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kV1LHDEUhoO04Nb6B7wa8KY3sfmYJDOXstQqWHqj1yGbnF2zzEzWnEzRf99s1yIVKSEkhOd5OeQl5IyzC86Y-Yqc6VZTJnjdrVa0OyILroykknHzgSxYryXtRS-OySfELWOsNy1bkLB0YYzzSOMUZg-hSU8xuBJ_QYMlA2ITp-YHZCg5PjXj38smDgM2A7iATUnNGEvyD2kKOTo6Qoiu1Ci3S7uSMOJn8nHtBoTTl_OE3F99u1te09uf32-Wl7fUt1oWKo3m3HVB8SCVCtw42QmvnQxMB-9Z503oPQjFV600CpTWADyAVmyljTPyhHw55O5yepwBix0jehgGN0Ga0Yr6Ia3UXS8rev4G3aY5T3W6SvW9qGBnXqmNG8DGaZ1Kdn4fai8Nl6ZVWnSVuniHqivAGH2aYB3r-z-COAg-J8QMa7vLcXT52XJm933aQ5-29mn_9Gn3kjxIWOFpA_l14v9YvwFYP6JN</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Wang, 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(London)</jtitle><stitle>Ecotoxicology</stitle><date>2021-12-01</date><risdate>2021</risdate><volume>30</volume><issue>10</issue><spage>2011</spage><epage>2023</epage><pages>2011-2023</pages><issn>0963-9292</issn><eissn>1573-3017</eissn><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
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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source | Springer Nature - Complete Springer Journals |
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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