Exploiting the Freshwater Shrimp Neocaridina denticulata as Aquatic Invertebrate Model to Evaluate Nontargeted Pesticide Induced Toxicity by Investigating Physiologic and Biochemical Parameters
As a nicotinoid neurotoxic insecticide, imidacloprid (IMI) works by disrupting nerve transmission via nicotinic acetylcholine receptor (nAChR). Although IMI is specifically targeting insects, nontarget animals such as the freshwater shrimp, Neocaridina denticulata, could also be affected, thus causi...
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Published in | Antioxidants Vol. 10; no. 3; p. 391 |
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Main Authors | , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Switzerland
MDPI AG
05.03.2021
MDPI |
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Online Access | Get full text |
ISSN | 2076-3921 2076-3921 |
DOI | 10.3390/antiox10030391 |
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Abstract | As a nicotinoid neurotoxic insecticide, imidacloprid (IMI) works by disrupting nerve transmission via nicotinic acetylcholine receptor (nAChR). Although IMI is specifically targeting insects, nontarget animals such as the freshwater shrimp, Neocaridina denticulata, could also be affected, thus causing adverse effects on the aquatic environment. To investigate IMI toxicity on nontarget organisms like N. denticulata, their physiology (locomotor activity, heartbeat, and gill ventilation) and biochemical factors (oxidative stress, energy metabolism) after IMI exposure were examined. IMI exposure at various concentrations (0.03125, 0.0625, 0.125, 0.25, 0.5, and 1 ppm) to shrimp after 24, 48, 72 h led to dramatic reduction of locomotor activity even at low concentrations. Meanwhile, IMI exposure after 92 h caused reduced heartbeat and gill ventilation at high concentrations. Biochemical assays were performed to investigate oxidative stress and energy metabolism. Interestingly, locomotion immobilization and cardiac activity were rescued after acetylcholine administration. Through molecular docking, IMI demonstrated high binding affinity to nAChR. Thus, locomotor activity and heartbeat in shrimp after IMI exposure may be caused by nAChR blockade and not alterations caused by oxidative stress and energy metabolism. To summarize, N. denticulata serves as an excellent and sensitive aquatic invertebrate model to conduct pesticide toxicity assays that encompass physiologic and biochemical examinations. |
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AbstractList | As a nicotinoid neurotoxic insecticide, imidacloprid (IMI) works by disrupting nerve transmission via nicotinic acetylcholine receptor (nAChR). Although IMI is specifically targeting insects, nontarget animals such as the freshwater shrimp, Neocaridina denticulata, could also be affected, thus causing adverse effects on the aquatic environment. To investigate IMI toxicity on nontarget organisms like N. denticulata, their physiology (locomotor activity, heartbeat, and gill ventilation) and biochemical factors (oxidative stress, energy metabolism) after IMI exposure were examined. IMI exposure at various concentrations (0.03125, 0.0625, 0.125, 0.25, 0.5, and 1 ppm) to shrimp after 24, 48, 72 h led to dramatic reduction of locomotor activity even at low concentrations. Meanwhile, IMI exposure after 92 h caused reduced heartbeat and gill ventilation at high concentrations. Biochemical assays were performed to investigate oxidative stress and energy metabolism. Interestingly, locomotion immobilization and cardiac activity were rescued after acetylcholine administration. Through molecular docking, IMI demonstrated high binding affinity to nAChR. Thus, locomotor activity and heartbeat in shrimp after IMI exposure may be caused by nAChR blockade and not alterations caused by oxidative stress and energy metabolism. To summarize, N. denticulata serves as an excellent and sensitive aquatic invertebrate model to conduct pesticide toxicity assays that encompass physiologic and biochemical examinations. As a nicotinoid neurotoxic insecticide, imidacloprid (IMI) works by disrupting nerve transmission via nicotinic acetylcholine receptor (nAChR). Although IMI is specifically targeting insects, nontarget animals such as the freshwater shrimp, Neocaridina denticulata, could also be affected, thus causing adverse effects on the aquatic environment. To investigate IMI toxicity on nontarget organisms like N. denticulata, their physiology (locomotor activity, heartbeat, and gill ventilation) and biochemical factors (oxidative stress, energy metabolism) after IMI exposure were examined. IMI exposure at various concentrations (0.03125, 0.0625, 0.125, 0.25, 0.5, and 1 ppm) to shrimp after 24, 48, 72 h led to dramatic reduction of locomotor activity even at low concentrations. Meanwhile, IMI exposure after 92 h caused reduced heartbeat and gill ventilation at high concentrations. Biochemical assays were performed to investigate oxidative stress and energy metabolism. Interestingly, locomotion immobilization and cardiac activity were rescued after acetylcholine administration. Through molecular docking, IMI demonstrated high binding affinity to nAChR. Thus, locomotor activity and heartbeat in shrimp after IMI exposure may be caused by nAChR blockade and not alterations caused by oxidative stress and energy metabolism. To summarize, N. denticulata serves as an excellent and sensitive aquatic invertebrate model to conduct pesticide toxicity assays that encompass physiologic and biochemical examinations.As a nicotinoid neurotoxic insecticide, imidacloprid (IMI) works by disrupting nerve transmission via nicotinic acetylcholine receptor (nAChR). Although IMI is specifically targeting insects, nontarget animals such as the freshwater shrimp, Neocaridina denticulata, could also be affected, thus causing adverse effects on the aquatic environment. To investigate IMI toxicity on nontarget organisms like N. denticulata, their physiology (locomotor activity, heartbeat, and gill ventilation) and biochemical factors (oxidative stress, energy metabolism) after IMI exposure were examined. IMI exposure at various concentrations (0.03125, 0.0625, 0.125, 0.25, 0.5, and 1 ppm) to shrimp after 24, 48, 72 h led to dramatic reduction of locomotor activity even at low concentrations. Meanwhile, IMI exposure after 92 h caused reduced heartbeat and gill ventilation at high concentrations. Biochemical assays were performed to investigate oxidative stress and energy metabolism. Interestingly, locomotion immobilization and cardiac activity were rescued after acetylcholine administration. Through molecular docking, IMI demonstrated high binding affinity to nAChR. Thus, locomotor activity and heartbeat in shrimp after IMI exposure may be caused by nAChR blockade and not alterations caused by oxidative stress and energy metabolism. To summarize, N. denticulata serves as an excellent and sensitive aquatic invertebrate model to conduct pesticide toxicity assays that encompass physiologic and biochemical examinations. As a nicotinoid neurotoxic insecticide, imidacloprid (IMI) works by disrupting nerve transmission via nicotinic acetylcholine receptor (nAChR). Although IMI is specifically targeting insects, nontarget animals such as the freshwater shrimp, Neocaridina denticulata , could also be affected, thus causing adverse effects on the aquatic environment. To investigate IMI toxicity on nontarget organisms like N. denticulata , their physiology (locomotor activity, heartbeat, and gill ventilation) and biochemical factors (oxidative stress, energy metabolism) after IMI exposure were examined. IMI exposure at various concentrations (0.03125, 0.0625, 0.125, 0.25, 0.5, and 1 ppm) to shrimp after 24, 48, 72 h led to dramatic reduction of locomotor activity even at low concentrations. Meanwhile, IMI exposure after 92 h caused reduced heartbeat and gill ventilation at high concentrations. Biochemical assays were performed to investigate oxidative stress and energy metabolism. Interestingly, locomotion immobilization and cardiac activity were rescued after acetylcholine administration. Through molecular docking, IMI demonstrated high binding affinity to nAChR. Thus, locomotor activity and heartbeat in shrimp after IMI exposure may be caused by nAChR blockade and not alterations caused by oxidative stress and energy metabolism. To summarize, N. denticulata serves as an excellent and sensitive aquatic invertebrate model to conduct pesticide toxicity assays that encompass physiologic and biochemical examinations. As a nicotinoid neurotoxic insecticide, imidacloprid (IMI) works by disrupting nerve transmission via nicotinic acetylcholine receptor (nAChR). Although IMI is specifically targeting insects, nontarget animals such as the freshwater shrimp, , could also be affected, thus causing adverse effects on the aquatic environment. To investigate IMI toxicity on nontarget organisms like , their physiology (locomotor activity, heartbeat, and gill ventilation) and biochemical factors (oxidative stress, energy metabolism) after IMI exposure were examined. IMI exposure at various concentrations (0.03125, 0.0625, 0.125, 0.25, 0.5, and 1 ppm) to shrimp after 24, 48, 72 h led to dramatic reduction of locomotor activity even at low concentrations. Meanwhile, IMI exposure after 92 h caused reduced heartbeat and gill ventilation at high concentrations. Biochemical assays were performed to investigate oxidative stress and energy metabolism. Interestingly, locomotion immobilization and cardiac activity were rescued after acetylcholine administration. Through molecular docking, IMI demonstrated high binding affinity to nAChR. Thus, locomotor activity and heartbeat in shrimp after IMI exposure may be caused by nAChR blockade and not alterations caused by oxidative stress and energy metabolism. To summarize, serves as an excellent and sensitive aquatic invertebrate model to conduct pesticide toxicity assays that encompass physiologic and biochemical examinations. |
Author | Fernandez, Rey Arturo Santoso, Fiorency Saputra, Ferry Suryanto, Michael Edbert Hsiao, Chung-Der Macabeo, Allan Patrick G. Audira, Gilbert Roldan, Marri Jmelou M. Hussain, Akhlaq Ngoc Hieu, Bui Thi Kurnia, Kevin Adi Lai, Hong-Thih Siregar, Petrus Huang, Jong-Chin Chen, Hong-Ming Chen, Kelvin H.-C. |
AuthorAffiliation | 7 Center for Nanotechnology, Chung Yuan Christian University, Chung-Li 320314, Taiwan 1 Department of Chemistry, Chung Yuan Christian University, Chung-Li 320314, Taiwan; g10765013@cycu.edu.tw (P.S.); hieubtn90@gmail.com (B.T.N.H.); g10701304@cycu.edu.tw (G.A.) 5 Faculty of Pharmacy and The Graduate School, University of Santo Tomas, Manila 1008, Philippines; mmroldan@ust.edu.ph 6 Laboratory for Organic Reactivity, Discovery and Synthesis (LORDS), Research Center for the Natural and Applied Sciences, University of Santo Tomas, Manila 1008, Philippines; reyarturo.tapia.fernandez@gmail.com 4 Department of Aquatic Biosciences, National Chiayi University, 300 University Rd., Chiayi 60004, Taiwan; wwwtt333@gmail.com 2 Department of Bioscience Technology, Chung Yuan Christian University, Chung-Li 320314, Taiwan; g10865014@cycu.edu.tw (M.E.S.); g10865016@cycu.edu.tw (K.A.K.); g10766011@cycu.edu.tw (F.S.); g10765017@cycu.edu.tw (A.H.); g10865013@cycu.edu.tw (F.S.) 3 Department of Applied Chemistry, |
AuthorAffiliation_xml | – name: 1 Department of Chemistry, Chung Yuan Christian University, Chung-Li 320314, Taiwan; g10765013@cycu.edu.tw (P.S.); hieubtn90@gmail.com (B.T.N.H.); g10701304@cycu.edu.tw (G.A.) – name: 3 Department of Applied Chemistry, National Pingtung University, Pingtung 900391, Taiwan; kelvin@mail.nptu.edu.tw (K.H.-C.C.); hjc@mail.nptu.edu.tw (J.-C.H.) – name: 4 Department of Aquatic Biosciences, National Chiayi University, 300 University Rd., Chiayi 60004, Taiwan; wwwtt333@gmail.com – name: 6 Laboratory for Organic Reactivity, Discovery and Synthesis (LORDS), Research Center for the Natural and Applied Sciences, University of Santo Tomas, Manila 1008, Philippines; reyarturo.tapia.fernandez@gmail.com – name: 5 Faculty of Pharmacy and The Graduate School, University of Santo Tomas, Manila 1008, Philippines; mmroldan@ust.edu.ph – name: 2 Department of Bioscience Technology, Chung Yuan Christian University, Chung-Li 320314, Taiwan; g10865014@cycu.edu.tw (M.E.S.); g10865016@cycu.edu.tw (K.A.K.); g10766011@cycu.edu.tw (F.S.); g10765017@cycu.edu.tw (A.H.); g10865013@cycu.edu.tw (F.S.) – name: 7 Center for Nanotechnology, Chung Yuan Christian University, Chung-Li 320314, Taiwan |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33807713$$D View this record in MEDLINE/PubMed |
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Keywords | Neocaridina denticulata shrimp cardiac activity insecticide locomotion activity ecotoxicity imidacloprid |
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Snippet | As a nicotinoid neurotoxic insecticide, imidacloprid (IMI) works by disrupting nerve transmission via nicotinic acetylcholine receptor (nAChR). Although IMI is... |
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SubjectTerms | acetylcholine Acetylcholine receptors (nicotinic) Aquatic environment cardiac activity Energy metabolism Experiments Freshwater resources Heart heart rate Imidacloprid Immobilization insecticide Insecticides Insects Invertebrates Locomotion locomotion activity Locomotor activity Neocaridina denticulata nerve tissue Nervous system Neurotoxicity Neurotransmission nicotinic receptors Nontarget organisms Oxidative metabolism Oxidative stress Pesticides shrimp Ventilation |
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Title | Exploiting the Freshwater Shrimp Neocaridina denticulata as Aquatic Invertebrate Model to Evaluate Nontargeted Pesticide Induced Toxicity by Investigating Physiologic and Biochemical Parameters |
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