Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster
The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as a...
Ausführliche Beschreibung
Autor*in: |
Qifang Wu [verfasserIn] Xueting Du [verfasserIn] Xucong Feng [verfasserIn] Huimin Cheng [verfasserIn] Yingjun Chen [verfasserIn] Chenying Lu [verfasserIn] Mingjiang Wu [verfasserIn] Haibin Tong [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2021 |
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Übergeordnetes Werk: |
In: Ecotoxicology and Environmental Safety - Elsevier, 2021, 225(2021), Seite 112739- |
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Übergeordnetes Werk: |
volume:225 ; year:2021 ; pages:112739- |
Links: |
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DOI / URN: |
10.1016/j.ecoenv.2021.112739 |
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Katalog-ID: |
DOAJ069209847 |
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520 | |a The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. Collectively, chlordane causes lipid peroxidation and disrupts redox homeostasis, which may be a potential mechanism leading to impaired insulin signaling and the metabolism of glucose and lipid, ultimately affects Drosophila development. | ||
650 | 4 | |a Chlordane | |
650 | 4 | |a Drosophila melanogaster | |
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10.1016/j.ecoenv.2021.112739 doi (DE-627)DOAJ069209847 (DE-599)DOAJ939138c4d31b4caf8a075c7b568df0f5 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 Qifang Wu verfasserin aut Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. Collectively, chlordane causes lipid peroxidation and disrupts redox homeostasis, which may be a potential mechanism leading to impaired insulin signaling and the metabolism of glucose and lipid, ultimately affects Drosophila development. Chlordane Drosophila melanogaster Glucose and lipid metabolism Oxidative stress Environmental pollution Environmental sciences Xueting Du verfasserin aut Xucong Feng verfasserin aut Huimin Cheng verfasserin aut Yingjun Chen verfasserin aut Chenying Lu verfasserin aut Mingjiang Wu verfasserin aut Haibin Tong verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 225(2021), Seite 112739- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:225 year:2021 pages:112739- https://doi.org/10.1016/j.ecoenv.2021.112739 kostenfrei https://doaj.org/article/939138c4d31b4caf8a075c7b568df0f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321008514 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 225 2021 112739- |
spelling |
10.1016/j.ecoenv.2021.112739 doi (DE-627)DOAJ069209847 (DE-599)DOAJ939138c4d31b4caf8a075c7b568df0f5 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 Qifang Wu verfasserin aut Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. Collectively, chlordane causes lipid peroxidation and disrupts redox homeostasis, which may be a potential mechanism leading to impaired insulin signaling and the metabolism of glucose and lipid, ultimately affects Drosophila development. Chlordane Drosophila melanogaster Glucose and lipid metabolism Oxidative stress Environmental pollution Environmental sciences Xueting Du verfasserin aut Xucong Feng verfasserin aut Huimin Cheng verfasserin aut Yingjun Chen verfasserin aut Chenying Lu verfasserin aut Mingjiang Wu verfasserin aut Haibin Tong verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 225(2021), Seite 112739- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:225 year:2021 pages:112739- https://doi.org/10.1016/j.ecoenv.2021.112739 kostenfrei https://doaj.org/article/939138c4d31b4caf8a075c7b568df0f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321008514 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 225 2021 112739- |
allfields_unstemmed |
10.1016/j.ecoenv.2021.112739 doi (DE-627)DOAJ069209847 (DE-599)DOAJ939138c4d31b4caf8a075c7b568df0f5 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 Qifang Wu verfasserin aut Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. Collectively, chlordane causes lipid peroxidation and disrupts redox homeostasis, which may be a potential mechanism leading to impaired insulin signaling and the metabolism of glucose and lipid, ultimately affects Drosophila development. Chlordane Drosophila melanogaster Glucose and lipid metabolism Oxidative stress Environmental pollution Environmental sciences Xueting Du verfasserin aut Xucong Feng verfasserin aut Huimin Cheng verfasserin aut Yingjun Chen verfasserin aut Chenying Lu verfasserin aut Mingjiang Wu verfasserin aut Haibin Tong verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 225(2021), Seite 112739- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:225 year:2021 pages:112739- https://doi.org/10.1016/j.ecoenv.2021.112739 kostenfrei https://doaj.org/article/939138c4d31b4caf8a075c7b568df0f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321008514 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 225 2021 112739- |
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10.1016/j.ecoenv.2021.112739 doi (DE-627)DOAJ069209847 (DE-599)DOAJ939138c4d31b4caf8a075c7b568df0f5 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 Qifang Wu verfasserin aut Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. Collectively, chlordane causes lipid peroxidation and disrupts redox homeostasis, which may be a potential mechanism leading to impaired insulin signaling and the metabolism of glucose and lipid, ultimately affects Drosophila development. Chlordane Drosophila melanogaster Glucose and lipid metabolism Oxidative stress Environmental pollution Environmental sciences Xueting Du verfasserin aut Xucong Feng verfasserin aut Huimin Cheng verfasserin aut Yingjun Chen verfasserin aut Chenying Lu verfasserin aut Mingjiang Wu verfasserin aut Haibin Tong verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 225(2021), Seite 112739- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:225 year:2021 pages:112739- https://doi.org/10.1016/j.ecoenv.2021.112739 kostenfrei https://doaj.org/article/939138c4d31b4caf8a075c7b568df0f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321008514 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 225 2021 112739- |
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10.1016/j.ecoenv.2021.112739 doi (DE-627)DOAJ069209847 (DE-599)DOAJ939138c4d31b4caf8a075c7b568df0f5 DE-627 ger DE-627 rakwb eng TD172-193.5 GE1-350 Qifang Wu verfasserin aut Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. Collectively, chlordane causes lipid peroxidation and disrupts redox homeostasis, which may be a potential mechanism leading to impaired insulin signaling and the metabolism of glucose and lipid, ultimately affects Drosophila development. Chlordane Drosophila melanogaster Glucose and lipid metabolism Oxidative stress Environmental pollution Environmental sciences Xueting Du verfasserin aut Xucong Feng verfasserin aut Huimin Cheng verfasserin aut Yingjun Chen verfasserin aut Chenying Lu verfasserin aut Mingjiang Wu verfasserin aut Haibin Tong verfasserin aut In Ecotoxicology and Environmental Safety Elsevier, 2021 225(2021), Seite 112739- (DE-627)266018467 (DE-600)1466969-9 10902414 nnns volume:225 year:2021 pages:112739- https://doi.org/10.1016/j.ecoenv.2021.112739 kostenfrei https://doaj.org/article/939138c4d31b4caf8a075c7b568df0f5 kostenfrei http://www.sciencedirect.com/science/article/pii/S0147651321008514 kostenfrei https://doaj.org/toc/0147-6513 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 225 2021 112739- |
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TD172-193.5 GE1-350 Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster Chlordane Drosophila melanogaster Glucose and lipid metabolism Oxidative stress |
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Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster |
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chlordane exposure causes developmental delay and metabolic disorders in drosophila melanogaster |
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Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster |
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The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. Collectively, chlordane causes lipid peroxidation and disrupts redox homeostasis, which may be a potential mechanism leading to impaired insulin signaling and the metabolism of glucose and lipid, ultimately affects Drosophila development. |
abstractGer |
The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. Collectively, chlordane causes lipid peroxidation and disrupts redox homeostasis, which may be a potential mechanism leading to impaired insulin signaling and the metabolism of glucose and lipid, ultimately affects Drosophila development. |
abstract_unstemmed |
The incidence of metabolic diseases is increasing every year, and several studies have highlighted the activity of persistent organic pollutants (POPs) in causing hyperlipidemia and diabetes, and these compounds are considered to be endocrine disrupting chemicals (EDCs). Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. Collectively, chlordane causes lipid peroxidation and disrupts redox homeostasis, which may be a potential mechanism leading to impaired insulin signaling and the metabolism of glucose and lipid, ultimately affects Drosophila development. |
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title_short |
Chlordane exposure causes developmental delay and metabolic disorders in Drosophila melanogaster |
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https://doi.org/10.1016/j.ecoenv.2021.112739 https://doaj.org/article/939138c4d31b4caf8a075c7b568df0f5 http://www.sciencedirect.com/science/article/pii/S0147651321008514 https://doaj.org/toc/0147-6513 |
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Chlordane is classified as an endocrine disruptor, but the mechanism of how it functions is still unclear. This study investigates the effects of chlordane exposure on Drosophila larvae. Drosophila was cultured in diet containing 0.01 μM, 0.1 μM, 1 μM, 5 μM, and 10 μM chlordane, and the toxicity of chlordane, the growth and development of Drosophila, the homeostasis of glucose and lipid metabolism and insulin signaling pathway, lipid peroxidation-related indicators and Nrf2 signaling pathway were evaluated. We here found that exposure to high concentrations of chlordane decreased the survival rate of Drosophila and that exposure to low concentrations of chlordane caused disruption of glucose and lipid metabolism, increased insulin secretion and impairment of insulin signaling. Notably, it also led to massive ROS production and lipid peroxidation despite of the activation of Nrf2 signaling pathway, an important pathway for maintaining redox homeostasis. 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code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Ecotoxicology and Environmental Safety</subfield><subfield code="d">Elsevier, 2021</subfield><subfield code="g">225(2021), Seite 112739-</subfield><subfield code="w">(DE-627)266018467</subfield><subfield code="w">(DE-600)1466969-9</subfield><subfield code="x">10902414</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:225</subfield><subfield code="g">year:2021</subfield><subfield code="g">pages:112739-</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.ecoenv.2021.112739</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doaj.org/article/939138c4d31b4caf8a075c7b568df0f5</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" ind1="4" 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