Paralysis caused by dinotefuran at environmental concentration via interfering the Ca 2+ -ROS-mitochondria pathway in Chironomus kiiensis
Dinotefuran as the third-generation of neonicotinoid insecticides is extensively used in agriculture worldwide, posing a potential toxic threat to non-target animals and humans. However, the chronic toxicity mechanism related to mitochondria damage of dinotefuran to non-target animals at environment...
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| creator | Wei, Fenghua Gu, Weiwen Zhang, Fengru Wu, Shuangxin |
| description | Dinotefuran as the third-generation of neonicotinoid insecticides is extensively used in agriculture worldwide, posing a potential toxic threat to non-target animals and humans. However, the chronic toxicity mechanism related to mitochondria damage of dinotefuran to non-target animals at environmental concentration is unclear.
In this study, the mitochondria damage and oxidative stress of dinotefuran on
were investigated at environmental concentrations by long-term exposure. At the same time, relevant gene expressions of these toxicity indexes were measured as sensitive ecotoxicity biomarkers to reflect the toxic effects of dinotefuran on Chironomidae.
Our present study showed that chronic exposure to environmental concentrations of dinotefuran resulted in behavioral inhibition in the larvae of Chironomidae. For burrowing inhibition of 10 days, the lowest observed-effect concentration (LOEC) and 50% inhibitory concentration (IC
) were 0.01 (0.01-0.04) and 0.60 (0.44-0.82) μg/L, respectively. Dinotefuran promoted the release of intracellular calcium ions (Ca
) in Chironomidae via dysregulating the gene expressions of
,
, and
. Subsequently, the disruption of the Ca
signaling pathway induced oxidative stress by raising reactive oxygen species (ROS), hydrogen peroxide (H
O
), and malonaldehyde (MDA) levels. Thus, the over-release of Ca
and ROS disordered the normal functioning of mitochondrial-related pathways by dysregulating the expressions of mitochondria-related genes of
,
, and
.
Our findings showed that low environmental concentrations of dinotefuran caused paralysis of the midge via interfering the Ca
-ROS-mitochondria pathway. These results provided data support for assessing the potential environmental risk of dinotefuran. |
| format | Article |
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In this study, the mitochondria damage and oxidative stress of dinotefuran on
were investigated at environmental concentrations by long-term exposure. At the same time, relevant gene expressions of these toxicity indexes were measured as sensitive ecotoxicity biomarkers to reflect the toxic effects of dinotefuran on Chironomidae.
Our present study showed that chronic exposure to environmental concentrations of dinotefuran resulted in behavioral inhibition in the larvae of Chironomidae. For burrowing inhibition of 10 days, the lowest observed-effect concentration (LOEC) and 50% inhibitory concentration (IC
) were 0.01 (0.01-0.04) and 0.60 (0.44-0.82) μg/L, respectively. Dinotefuran promoted the release of intracellular calcium ions (Ca
) in Chironomidae via dysregulating the gene expressions of
,
, and
. Subsequently, the disruption of the Ca
signaling pathway induced oxidative stress by raising reactive oxygen species (ROS), hydrogen peroxide (H
O
), and malonaldehyde (MDA) levels. Thus, the over-release of Ca
and ROS disordered the normal functioning of mitochondrial-related pathways by dysregulating the expressions of mitochondria-related genes of
,
, and
.
Our findings showed that low environmental concentrations of dinotefuran caused paralysis of the midge via interfering the Ca
-ROS-mitochondria pathway. These results provided data support for assessing the potential environmental risk of dinotefuran.</description><identifier>EISSN: 2296-2565</identifier><identifier>PMID: 39416932</identifier><language>eng</language><publisher>Switzerland</publisher><subject>Animals ; Calcium - metabolism ; Chironomidae - drug effects ; Guanidines - toxicity ; Insecticides - toxicity ; Larva - drug effects ; Mitochondria - drug effects ; Mitochondria - metabolism ; Neonicotinoids - toxicity ; Nitro Compounds - toxicity ; Oxidative Stress - drug effects ; Reactive Oxygen Species - metabolism</subject><ispartof>Frontiers in public health, 2024, Vol.12, p.1468384</ispartof><rights>Copyright © 2024 Wei, Gu, Zhang and Wu.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39416932$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wei, Fenghua</creatorcontrib><creatorcontrib>Gu, Weiwen</creatorcontrib><creatorcontrib>Zhang, Fengru</creatorcontrib><creatorcontrib>Wu, Shuangxin</creatorcontrib><title>Paralysis caused by dinotefuran at environmental concentration via interfering the Ca 2+ -ROS-mitochondria pathway in Chironomus kiiensis</title><title>Frontiers in public health</title><addtitle>Front Public Health</addtitle><description>Dinotefuran as the third-generation of neonicotinoid insecticides is extensively used in agriculture worldwide, posing a potential toxic threat to non-target animals and humans. However, the chronic toxicity mechanism related to mitochondria damage of dinotefuran to non-target animals at environmental concentration is unclear.
In this study, the mitochondria damage and oxidative stress of dinotefuran on
were investigated at environmental concentrations by long-term exposure. At the same time, relevant gene expressions of these toxicity indexes were measured as sensitive ecotoxicity biomarkers to reflect the toxic effects of dinotefuran on Chironomidae.
Our present study showed that chronic exposure to environmental concentrations of dinotefuran resulted in behavioral inhibition in the larvae of Chironomidae. For burrowing inhibition of 10 days, the lowest observed-effect concentration (LOEC) and 50% inhibitory concentration (IC
) were 0.01 (0.01-0.04) and 0.60 (0.44-0.82) μg/L, respectively. Dinotefuran promoted the release of intracellular calcium ions (Ca
) in Chironomidae via dysregulating the gene expressions of
,
, and
. Subsequently, the disruption of the Ca
signaling pathway induced oxidative stress by raising reactive oxygen species (ROS), hydrogen peroxide (H
O
), and malonaldehyde (MDA) levels. Thus, the over-release of Ca
and ROS disordered the normal functioning of mitochondrial-related pathways by dysregulating the expressions of mitochondria-related genes of
,
, and
.
Our findings showed that low environmental concentrations of dinotefuran caused paralysis of the midge via interfering the Ca
-ROS-mitochondria pathway. These results provided data support for assessing the potential environmental risk of dinotefuran.</description><subject>Animals</subject><subject>Calcium - metabolism</subject><subject>Chironomidae - drug effects</subject><subject>Guanidines - toxicity</subject><subject>Insecticides - toxicity</subject><subject>Larva - drug effects</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Neonicotinoids - toxicity</subject><subject>Nitro Compounds - toxicity</subject><subject>Oxidative Stress - drug effects</subject><subject>Reactive Oxygen Species - metabolism</subject><issn>2296-2565</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFjkFLw0AQhRdBbLH9CzJ3CWw2bSDnoHhT1HuZJhMzbXY2zG4q-Qn-ayPo2dN7h4_vvSuzdq4qM7cv9yuzjfFkrc1tsbMuvzGrotrlZVW4tfl6QcVhjhyhwSlSC8cZWpaQqJsUBTAByYU1iCdJOEATpFmaYuIgcGEElkTakbJ8QOoJagR3D9nr81vmOYWmD9Lqwo2Y-k-cFx7q_scY_BThzEyy7G_MdYdDpO1v3pq7x4f3-ikbp6On9jAqe9T58Pe9-Bf4Bg4BUpk</recordid><startdate>2024</startdate><enddate>2024</enddate><creator>Wei, Fenghua</creator><creator>Gu, Weiwen</creator><creator>Zhang, Fengru</creator><creator>Wu, Shuangxin</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>2024</creationdate><title>Paralysis caused by dinotefuran at environmental concentration via interfering the Ca 2+ -ROS-mitochondria pathway in Chironomus kiiensis</title><author>Wei, Fenghua ; Gu, Weiwen ; Zhang, Fengru ; Wu, Shuangxin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmed_primary_394169323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Calcium - metabolism</topic><topic>Chironomidae - drug effects</topic><topic>Guanidines - toxicity</topic><topic>Insecticides - toxicity</topic><topic>Larva - drug effects</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Neonicotinoids - toxicity</topic><topic>Nitro Compounds - toxicity</topic><topic>Oxidative Stress - drug effects</topic><topic>Reactive Oxygen Species - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wei, Fenghua</creatorcontrib><creatorcontrib>Gu, Weiwen</creatorcontrib><creatorcontrib>Zhang, Fengru</creatorcontrib><creatorcontrib>Wu, Shuangxin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Frontiers in public health</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wei, Fenghua</au><au>Gu, Weiwen</au><au>Zhang, Fengru</au><au>Wu, Shuangxin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Paralysis caused by dinotefuran at environmental concentration via interfering the Ca 2+ -ROS-mitochondria pathway in Chironomus kiiensis</atitle><jtitle>Frontiers in public health</jtitle><addtitle>Front Public Health</addtitle><date>2024</date><risdate>2024</risdate><volume>12</volume><spage>1468384</spage><pages>1468384-</pages><eissn>2296-2565</eissn><abstract>Dinotefuran as the third-generation of neonicotinoid insecticides is extensively used in agriculture worldwide, posing a potential toxic threat to non-target animals and humans. However, the chronic toxicity mechanism related to mitochondria damage of dinotefuran to non-target animals at environmental concentration is unclear.
In this study, the mitochondria damage and oxidative stress of dinotefuran on
were investigated at environmental concentrations by long-term exposure. At the same time, relevant gene expressions of these toxicity indexes were measured as sensitive ecotoxicity biomarkers to reflect the toxic effects of dinotefuran on Chironomidae.
Our present study showed that chronic exposure to environmental concentrations of dinotefuran resulted in behavioral inhibition in the larvae of Chironomidae. For burrowing inhibition of 10 days, the lowest observed-effect concentration (LOEC) and 50% inhibitory concentration (IC
) were 0.01 (0.01-0.04) and 0.60 (0.44-0.82) μg/L, respectively. Dinotefuran promoted the release of intracellular calcium ions (Ca
) in Chironomidae via dysregulating the gene expressions of
,
, and
. Subsequently, the disruption of the Ca
signaling pathway induced oxidative stress by raising reactive oxygen species (ROS), hydrogen peroxide (H
O
), and malonaldehyde (MDA) levels. Thus, the over-release of Ca
and ROS disordered the normal functioning of mitochondrial-related pathways by dysregulating the expressions of mitochondria-related genes of
,
, and
.
Our findings showed that low environmental concentrations of dinotefuran caused paralysis of the midge via interfering the Ca
-ROS-mitochondria pathway. These results provided data support for assessing the potential environmental risk of dinotefuran.</abstract><cop>Switzerland</cop><pmid>39416932</pmid></addata></record> |
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| ispartof | Frontiers in public health, 2024, Vol.12, p.1468384 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animals Calcium - metabolism Chironomidae - drug effects Guanidines - toxicity Insecticides - toxicity Larva - drug effects Mitochondria - drug effects Mitochondria - metabolism Neonicotinoids - toxicity Nitro Compounds - toxicity Oxidative Stress - drug effects Reactive Oxygen Species - metabolism |
| title | Paralysis caused by dinotefuran at environmental concentration via interfering the Ca 2+ -ROS-mitochondria pathway in Chironomus kiiensis |
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