Mercuric chloride‐induced oxidative stress, genotoxicity, haematological changes and histopathological alterations in fish Channa punctatus (Bloch, 1793)

The present study was undertaken to investigate the adverse effects of mercuric chloride (HgCl2) overload in the fish Channa punctatus. Two sublethal test concentrations of HgCl2 (1/20th and 1/10th of 96 h LC50 i.e., 0.03 mg l−1 (low concentration) and 0.07 mg l−1 (high concentration), respectively,...

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Published in:Journal of fish biology 2022-04, Vol.100 (4), p.868-883
Main Authors: Trivedi, Sunil P., Singh, Shefalee, Trivedi, Abha, Kumar, Manoj
Format: Article
Language:English
Subjects:
Abnormalities
Animals
Antioxidants
Antioxidants - metabolism
Antioxidants - pharmacology
Biological stress
Catalase
Channa punctata
Chlorides
DNA Damage
Enzymatic activity
Enzyme activity
Erythrocytes
Exposure
Fish
Fishes - genetics
Genotoxicity
Glutathione
Glutathione - genetics
Glutathione - metabolism
Glutathione - pharmacology
Glutathione reductase
haematological changes
Hematology
histopathological alterations
Histopathology
Kidneys
Lipid Peroxidation
Liver
Malformations
Manganese
Mercuric chloride
Mercuric Chloride - toxicity
mercury chloride
Mercury compounds
Micronuclei
Mortality causes
Oxidative stress
Oxidative Stress - genetics
Reductases
Superoxide dismutase
Superoxide Dismutase - genetics
Superoxide Dismutase - metabolism
Superoxide Dismutase - pharmacology
Tissue
Toxicity tests
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description The present study was undertaken to investigate the adverse effects of mercuric chloride (HgCl2) overload in the fish Channa punctatus. Two sublethal test concentrations of HgCl2 (1/20th and 1/10th of 96 h LC50 i.e., 0.03 mg l−1 (low concentration) and 0.07 mg l−1 (high concentration), respectively, were used for exposure. Blood, liver and kidney tissues of the control and exposed specimens were sampled at intervals of 15, 30, and 45 days to assess alterations in oxidative stress, genotoxicity haematological parameters and histopathology. Significant changes in Hb%, RBC count, WBC count, antioxidant enzyme activity, i.e., superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione reductase (GR), were recorded. Micronuclei (MN) induction, nuclear abnormalities (NAs) and histopathological alterations were also observed in the exposed fish. Significant (P 
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Two sublethal test concentrations of HgCl2 (1/20th and 1/10th of 96 h LC50 i.e., 0.03 mg l−1 (low concentration) and 0.07 mg l−1 (high concentration), respectively, were used for exposure. Blood, liver and kidney tissues of the control and exposed specimens were sampled at intervals of 15, 30, and 45 days to assess alterations in oxidative stress, genotoxicity haematological parameters and histopathology. Significant changes in Hb%, RBC count, WBC count, antioxidant enzyme activity, i.e., superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione reductase (GR), were recorded. Micronuclei (MN) induction, nuclear abnormalities (NAs) and histopathological alterations were also observed in the exposed fish. Significant (P &lt; 0.05) increase in the activities of SOD, CAT, GSH and GR was observed. After 45 days, a decrease in the level of GSH and GR was noticed which suggests an undermined anti‐oxidative defence system in the fish exposed to HgCl2. Histological examination of the liver and kidney showed serious tissue injury and histological alterations. Significant increases in MN and NA frequencies reveal the DNA damage in erythrocytes of fish, and haematological changes show the toxicological potential of HgCl2. 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Two sublethal test concentrations of HgCl2 (1/20th and 1/10th of 96 h LC50 i.e., 0.03 mg l−1 (low concentration) and 0.07 mg l−1 (high concentration), respectively, were used for exposure. Blood, liver and kidney tissues of the control and exposed specimens were sampled at intervals of 15, 30, and 45 days to assess alterations in oxidative stress, genotoxicity haematological parameters and histopathology. Significant changes in Hb%, RBC count, WBC count, antioxidant enzyme activity, i.e., superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione reductase (GR), were recorded. Micronuclei (MN) induction, nuclear abnormalities (NAs) and histopathological alterations were also observed in the exposed fish. Significant (P &lt; 0.05) increase in the activities of SOD, CAT, GSH and GR was observed. After 45 days, a decrease in the level of GSH and GR was noticed which suggests an undermined anti‐oxidative defence system in the fish exposed to HgCl2. Histological examination of the liver and kidney showed serious tissue injury and histological alterations. Significant increases in MN and NA frequencies reveal the DNA damage in erythrocytes of fish, and haematological changes show the toxicological potential of HgCl2. The observed changes in the antioxidant defence system, genotoxicity and haematological and histological changes in the present study provide the most extensive insight into HgCl2 stress in C. punctatus.</description><subject>Abnormalities</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Antioxidants - pharmacology</subject><subject>Biological stress</subject><subject>Catalase</subject><subject>Channa punctata</subject><subject>Chlorides</subject><subject>DNA Damage</subject><subject>Enzymatic activity</subject><subject>Enzyme activity</subject><subject>Erythrocytes</subject><subject>Exposure</subject><subject>Fish</subject><subject>Fishes - genetics</subject><subject>Genotoxicity</subject><subject>Glutathione</subject><subject>Glutathione - genetics</subject><subject>Glutathione - metabolism</subject><subject>Glutathione - pharmacology</subject><subject>Glutathione reductase</subject><subject>haematological changes</subject><subject>Hematology</subject><subject>histopathological alterations</subject><subject>Histopathology</subject><subject>Kidneys</subject><subject>Lipid Peroxidation</subject><subject>Liver</subject><subject>Malformations</subject><subject>Manganese</subject><subject>Mercuric chloride</subject><subject>Mercuric Chloride - toxicity</subject><subject>mercury chloride</subject><subject>Mercury compounds</subject><subject>Micronuclei</subject><subject>Mortality causes</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - genetics</subject><subject>Reductases</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxide Dismutase - pharmacology</subject><subject>Tissue</subject><subject>Toxicity tests</subject><issn>0022-1112</issn><issn>1095-8649</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp1kc1uEzEQxy0EoqFw4AWQJS6tlG3tdbxrH2lE-VARFziv_DGbdeTYwfYCufEI3Hk7ngRDSg9IzGWkmd_8NNIfoaeUXNBal9tRX1BOqLyHFpRI3ohuJe-jBSFt21SgPUGPct4SQiST7CE6YZxKLglfoB_vIJk5OYPN5GNyFn5---6CnQ1YHL86q4r7DDiXBDkv8QZCLHVsXDks8aRgp0r0ceOM8tWgwgYyVsHiyeUS96pMd1vlC6RqiyFjF_Do8oTX9SIovJ-DKarMGZ9d-WimJaa9ZOeP0YNR-QxPbvsp-nj98sP6dXPz_tWb9YubxjAhZCOk6oUmvQYgsiO2ta2gWjMuLGgtBTWMA2gJHXBKO9VKtRJihH7slWWjYKfo7Ojdp_hphlyGncsGvFcB4pyHtmMtXUnKeUWf_4Nu45xC_a5SnK9aSgmt1PmRMinmnGAc9sntVDoMlAy_ExtqYsOfxCr77NY46x3YO_JvRBW4PAJfnIfD_03D2-uro_IX29Oi2A</recordid><startdate>202204</startdate><enddate>202204</enddate><creator>Trivedi, Sunil P.</creator><creator>Singh, Shefalee</creator><creator>Trivedi, Abha</creator><creator>Kumar, Manoj</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7SN</scope><scope>7TN</scope><scope>8FD</scope><scope>C1K</scope><scope>F1W</scope><scope>FR3</scope><scope>H95</scope><scope>L.G</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9895-0685</orcidid></search><sort><creationdate>202204</creationdate><title>Mercuric chloride‐induced oxidative stress, genotoxicity, haematological changes and histopathological alterations in fish Channa punctatus (Bloch, 1793)</title><author>Trivedi, Sunil P. ; 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Histological examination of the liver and kidney showed serious tissue injury and histological alterations. Significant increases in MN and NA frequencies reveal the DNA damage in erythrocytes of fish, and haematological changes show the toxicological potential of HgCl2. The observed changes in the antioxidant defence system, genotoxicity and haematological and histological changes in the present study provide the most extensive insight into HgCl2 stress in C. punctatus.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>35195905</pmid><doi>10.1111/jfb.15019</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0001-9895-0685</orcidid><oa>free_for_read</oa></addata></record>
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subjects Abnormalities
Animals
Antioxidants
Antioxidants - metabolism
Antioxidants - pharmacology
Biological stress
Catalase
Channa punctata
Chlorides
DNA Damage
Enzymatic activity
Enzyme activity
Erythrocytes
Exposure
Fish
Fishes - genetics
Genotoxicity
Glutathione
Glutathione - genetics
Glutathione - metabolism
Glutathione - pharmacology
Glutathione reductase
haematological changes
Hematology
histopathological alterations
Histopathology
Kidneys
Lipid Peroxidation
Liver
Malformations
Manganese
Mercuric chloride
Mercuric Chloride - toxicity
mercury chloride
Mercury compounds
Micronuclei
Mortality causes
Oxidative stress
Oxidative Stress - genetics
Reductases
Superoxide dismutase
Superoxide Dismutase - genetics
Superoxide Dismutase - metabolism
Superoxide Dismutase - pharmacology
Tissue
Toxicity tests
title Mercuric chloride‐induced oxidative stress, genotoxicity, haematological changes and histopathological alterations in fish Channa punctatus (Bloch, 1793)
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