Effect of low-dose exposure of aluminium oxide nanoparticles in Swiss albino mice: Histopathological changes and oxidative damage
Rapid growth in the use of aluminium oxide nanoparticles (Al2O3 NPs) in various fields such as medicine, pharmacy, cosmetic industries, and engineering creates concerns since the literature is replete with data regarding their toxicity in living organisms. The objective of the present study was to d...
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description | Rapid growth in the use of aluminium oxide nanoparticles (Al2O3 NPs) in various fields such as medicine, pharmacy, cosmetic industries, and engineering creates concerns since the literature is replete with data regarding their toxicity in living organisms. The objective of the present study was to demonstrate the potential toxicological manifestations of repeated exposure to Al2O3 NP at low doses in vivo. In the present study, Al2O3 NP was orally administered at 15, 30 or 60 mg kg−1 body weight for 5 days to Swiss albino male mice. A battery of well-defined assays was undertaken to evaluate aluminium (Al) bioaccumulation, haematological and histological changes, oxidative damage and genotoxicity. Physico-chemical characterisation demonstrated increases in hydrodynamic diameter along the concentration gradient of Al2O3 NP dispersed in MilliQ water. Brain, liver, spleen, kidney and testes showed high Al retention levels. Histopathological lesions were prominent in the brain and liver. Al2O3 NP treatment increased levels of lipid peroxidation and decreased glutathione content in the test organs at all dose levels. The enzyme activities of catalase and superoxide dismutase were also significantly altered. DNA damage quantified using the comet assay was markedly increased in all the soft organs studied. Anatomical abnormalities, redox imbalance and DNA damage were positively correlated with Al retention in the respective organs. Size, zeta potential and colloidal state might have contributed to the bio-physico-chemical interactions of the NPs in vivo and were responsible for the non-linear dose response. The overall data indicate that Al2O3 NP exposure may result in adverse health consequences, inclusive of but not limited to disturbed redox homeostasis, hepatocellular toxicity, neurodegeneration and DNA damage. |
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The objective of the present study was to demonstrate the potential toxicological manifestations of repeated exposure to Al2O3 NP at low doses in vivo. In the present study, Al2O3 NP was orally administered at 15, 30 or 60 mg kg−1 body weight for 5 days to Swiss albino male mice. A battery of well-defined assays was undertaken to evaluate aluminium (Al) bioaccumulation, haematological and histological changes, oxidative damage and genotoxicity. Physico-chemical characterisation demonstrated increases in hydrodynamic diameter along the concentration gradient of Al2O3 NP dispersed in MilliQ water. Brain, liver, spleen, kidney and testes showed high Al retention levels. Histopathological lesions were prominent in the brain and liver. Al2O3 NP treatment increased levels of lipid peroxidation and decreased glutathione content in the test organs at all dose levels. The enzyme activities of catalase and superoxide dismutase were also significantly altered. DNA damage quantified using the comet assay was markedly increased in all the soft organs studied. Anatomical abnormalities, redox imbalance and DNA damage were positively correlated with Al retention in the respective organs. Size, zeta potential and colloidal state might have contributed to the bio-physico-chemical interactions of the NPs in vivo and were responsible for the non-linear dose response. The overall data indicate that Al2O3 NP exposure may result in adverse health consequences, inclusive of but not limited to disturbed redox homeostasis, hepatocellular toxicity, neurodegeneration and DNA damage.</description><identifier>ISSN: 0748-2337</identifier><identifier>EISSN: 1477-0393</identifier><identifier>DOI: 10.1177/0748233720936828</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Abnormalities ; Albinism ; Aluminum ; Aluminum oxide ; Bioaccumulation ; Bioassays ; Biocompatibility ; Body weight ; Brain ; Catalase ; Chemical damage ; Chemical interactions ; Comet assay ; Concentration gradient ; Damage detection ; Deoxyribonucleic acid ; DNA ; DNA damage ; Enzymatic activity ; Exposure ; Genotoxicity ; Glutathione ; Hematology ; Homeostasis ; In vivo methods and tests ; Kidneys ; Lipid peroxidation ; Lipids ; Liver ; Nanoparticles ; Neurodegeneration ; Nonlinear response ; Oral administration ; Organs ; Peroxidation ; Retention ; Spleen ; Superoxide dismutase ; Toxicity ; Zeta potential</subject><ispartof>Toxicology and industrial health, 2020-08, Vol.36 (8), p.567-579</ispartof><rights>The Author(s) 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c342t-19ced6cb44e28a32f8d80a455568d6104e18a9262278ef328e134bc9524bcfbc3</citedby><cites>FETCH-LOGICAL-c342t-19ced6cb44e28a32f8d80a455568d6104e18a9262278ef328e134bc9524bcfbc3</cites><orcidid>0000-0003-2071-6770</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0748233720936828$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0748233720936828$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,776,780,21799,27903,27904,43600,43601</link.rule.ids></links><search><creatorcontrib>De, Arpita</creatorcontrib><creatorcontrib>Ghosh, Swarupa</creatorcontrib><creatorcontrib>Chakrabarti, Manoswini</creatorcontrib><creatorcontrib>Ghosh, Ilika</creatorcontrib><creatorcontrib>Banerjee, Ritesh</creatorcontrib><creatorcontrib>Mukherjee, Anita</creatorcontrib><title>Effect of low-dose exposure of aluminium oxide nanoparticles in Swiss albino mice: Histopathological changes and oxidative damage</title><title>Toxicology and industrial health</title><addtitle>Toxicol Ind Health</addtitle><description>Rapid growth in the use of aluminium oxide nanoparticles (Al2O3 NPs) in various fields such as medicine, pharmacy, cosmetic industries, and engineering creates concerns since the literature is replete with data regarding their toxicity in living organisms. The objective of the present study was to demonstrate the potential toxicological manifestations of repeated exposure to Al2O3 NP at low doses in vivo. In the present study, Al2O3 NP was orally administered at 15, 30 or 60 mg kg−1 body weight for 5 days to Swiss albino male mice. A battery of well-defined assays was undertaken to evaluate aluminium (Al) bioaccumulation, haematological and histological changes, oxidative damage and genotoxicity. Physico-chemical characterisation demonstrated increases in hydrodynamic diameter along the concentration gradient of Al2O3 NP dispersed in MilliQ water. Brain, liver, spleen, kidney and testes showed high Al retention levels. Histopathological lesions were prominent in the brain and liver. Al2O3 NP treatment increased levels of lipid peroxidation and decreased glutathione content in the test organs at all dose levels. The enzyme activities of catalase and superoxide dismutase were also significantly altered. DNA damage quantified using the comet assay was markedly increased in all the soft organs studied. Anatomical abnormalities, redox imbalance and DNA damage were positively correlated with Al retention in the respective organs. Size, zeta potential and colloidal state might have contributed to the bio-physico-chemical interactions of the NPs in vivo and were responsible for the non-linear dose response. The overall data indicate that Al2O3 NP exposure may result in adverse health consequences, inclusive of but not limited to disturbed redox homeostasis, hepatocellular toxicity, neurodegeneration and DNA damage.</description><subject>Abnormalities</subject><subject>Albinism</subject><subject>Aluminum</subject><subject>Aluminum oxide</subject><subject>Bioaccumulation</subject><subject>Bioassays</subject><subject>Biocompatibility</subject><subject>Body weight</subject><subject>Brain</subject><subject>Catalase</subject><subject>Chemical damage</subject><subject>Chemical interactions</subject><subject>Comet assay</subject><subject>Concentration gradient</subject><subject>Damage detection</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>Enzymatic activity</subject><subject>Exposure</subject><subject>Genotoxicity</subject><subject>Glutathione</subject><subject>Hematology</subject><subject>Homeostasis</subject><subject>In vivo methods and tests</subject><subject>Kidneys</subject><subject>Lipid peroxidation</subject><subject>Lipids</subject><subject>Liver</subject><subject>Nanoparticles</subject><subject>Neurodegeneration</subject><subject>Nonlinear response</subject><subject>Oral administration</subject><subject>Organs</subject><subject>Peroxidation</subject><subject>Retention</subject><subject>Spleen</subject><subject>Superoxide dismutase</subject><subject>Toxicity</subject><subject>Zeta potential</subject><issn>0748-2337</issn><issn>1477-0393</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp1kM1Lw0AQxRdRsFbvHhc8R_crycablGqFggf1HDabSbsl2a27ia1H_3M3VhAELzMw7zdvmIfQJSXXlOb5DcmFZJznjBQ8k0weoQkVeZ4QXvBjNBnlZNRP0VkIG0JIlqVsgj7nTQO6x67BrdsltQuAYb91YfAwDlU7dMaaocNub2rAVlm3Vb43uoWAjcXPOxNCxCpjHe6Mhlu8MKGPUL92rVsZrVqs18quIq9s_e2jevMOuFadWsE5OmlUG-Dip0_R6_38ZbZIlk8Pj7O7ZaK5YH1CCw11pishgEnFWSNrSZRI0zSTdUaJACpVwTLGcgkNZxIoF5UuUhZrU2k-RVcH3613bwOEvty4wdt4smQipSnNZUYjRQ6U9i4ED0259aZT_qOkpByDLv8GHVeSw0qI3_ya_st_AeZJfvs</recordid><startdate>202008</startdate><enddate>202008</enddate><creator>De, Arpita</creator><creator>Ghosh, Swarupa</creator><creator>Chakrabarti, Manoswini</creator><creator>Ghosh, Ilika</creator><creator>Banerjee, Ritesh</creator><creator>Mukherjee, Anita</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QF</scope><scope>7QQ</scope><scope>7SC</scope><scope>7SE</scope><scope>7SP</scope><scope>7SR</scope><scope>7T2</scope><scope>7TA</scope><scope>7TB</scope><scope>7U5</scope><scope>7U7</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><orcidid>https://orcid.org/0000-0003-2071-6770</orcidid></search><sort><creationdate>202008</creationdate><title>Effect of low-dose exposure of aluminium oxide nanoparticles in Swiss albino mice: Histopathological changes and oxidative damage</title><author>De, Arpita ; 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The objective of the present study was to demonstrate the potential toxicological manifestations of repeated exposure to Al2O3 NP at low doses in vivo. In the present study, Al2O3 NP was orally administered at 15, 30 or 60 mg kg−1 body weight for 5 days to Swiss albino male mice. A battery of well-defined assays was undertaken to evaluate aluminium (Al) bioaccumulation, haematological and histological changes, oxidative damage and genotoxicity. Physico-chemical characterisation demonstrated increases in hydrodynamic diameter along the concentration gradient of Al2O3 NP dispersed in MilliQ water. Brain, liver, spleen, kidney and testes showed high Al retention levels. Histopathological lesions were prominent in the brain and liver. Al2O3 NP treatment increased levels of lipid peroxidation and decreased glutathione content in the test organs at all dose levels. The enzyme activities of catalase and superoxide dismutase were also significantly altered. DNA damage quantified using the comet assay was markedly increased in all the soft organs studied. Anatomical abnormalities, redox imbalance and DNA damage were positively correlated with Al retention in the respective organs. Size, zeta potential and colloidal state might have contributed to the bio-physico-chemical interactions of the NPs in vivo and were responsible for the non-linear dose response. The overall data indicate that Al2O3 NP exposure may result in adverse health consequences, inclusive of but not limited to disturbed redox homeostasis, hepatocellular toxicity, neurodegeneration and DNA damage.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><doi>10.1177/0748233720936828</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-2071-6770</orcidid></addata></record> |
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subjects | Abnormalities Albinism Aluminum Aluminum oxide Bioaccumulation Bioassays Biocompatibility Body weight Brain Catalase Chemical damage Chemical interactions Comet assay Concentration gradient Damage detection Deoxyribonucleic acid DNA DNA damage Enzymatic activity Exposure Genotoxicity Glutathione Hematology Homeostasis In vivo methods and tests Kidneys Lipid peroxidation Lipids Liver Nanoparticles Neurodegeneration Nonlinear response Oral administration Organs Peroxidation Retention Spleen Superoxide dismutase Toxicity Zeta potential |
title | Effect of low-dose exposure of aluminium oxide nanoparticles in Swiss albino mice: Histopathological changes and oxidative damage |
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