Resveratrol protects against cadmium‐induced cerebrum toxicity through modifications of the cytochrome P450 enzyme system in microsomes

BACKGROUND Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood–brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which leads to lethal cerebral edema, intracellular accumulation and cellular dysfunction, remains to be illuminated with regard to the...

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Published inJournal of the science of food and agriculture Vol. 103; no. 12; pp. 5883 - 5892
Main Authors Lv, Mei‐Wei, Zhang, Cong, Ge, Jing, Sun, Xiao‐Han, Li, Jin‐Yang, Li, Jin‐Long
Format Journal Article
LanguageEnglish
Published Chichester, UK John Wiley & Sons, Ltd 01.09.2023
John Wiley and Sons, Limited
Subjects
agriculture
AHR/CAR/PXR pathway
Alkanes
Blood-brain barrier
Cadmium
Cadmium - metabolism
Cadmium - toxicity
Cerebrum
Cerebrum - metabolism
chickens
Contaminants
cortex
CYP450
Cytochrome
cytochrome P-450
Cytochrome P-450 Enzyme System - genetics
Cytochrome P-450 Enzyme System - metabolism
Cytochrome P-450 Enzyme System - pharmacology
Cytochrome P450
Cytochromes P450
Damage accumulation
Degeneration
Edema
Enzymes
Gene expression
Glial cells
Granule cells
Metabolism
Microsomes
Microsomes - metabolism
Molecular modelling
Neurodegeneration
Neuronal-glial interactions
Neuroprotection
neuroprotective effect
neurotoxicity
Nuclear receptors
NXRs
Oxidative Stress
poisoning
pregnancy
Receptors
Receptors, Cytoplasmic and Nuclear - metabolism
Resveratrol
Resveratrol - metabolism
Resveratrol - pharmacology
Toxicity
Toxicosis
vacuoles
xenobiotics
cadmium
neurotoxicity
AHR/CAR/PXR pathway
CYP450
resveratrol
NXRs
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Abstract BACKGROUND Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood–brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which leads to lethal cerebral edema, intracellular accumulation and cellular dysfunction, remains to be illuminated with regard to the exact molecular mechanism of cerebral toxicity. Resveratrol (RES), present in the edible portions of numerous plants, is a simply acquirable and correspondingly less toxic natural compound with neuroprotective potential, which provides some theoretical bases for antagonizing Cd‐induced cerebral toxicity. RESULTS This work was executed to research the protective effects of RES against Cd‐induced toxicity in chicken cerebrum. Markedly, these lesions were increased in the Cd group, which also exhibited a thinner cortex, reduced granule cells, vacuolar degeneration, and an enlarged medullary space in the cerebrum. Furthermore, Cd induced CYP450 enzyme metabolism disorders by disrupting the nuclear xenobiotic receptor response (NXRs), enabling the cerebrum to reduce the ability to metabolize exogenous substances, eventually leading to Cd accumulation. Meanwhile, accumulated Cd promoted oxidative damage and synergistically promoted the damage to neurons and glial cells. CONCLUSION RES initiated NXRs (especially for aromatic receptor and pregnancy alkane X receptor), decreasing the expression of CYP450 genes, changing the content of CYP450, maintaining CYP450 enzyme normal activities, and exerting antagonistic action against the Cd‐induced abnormal response of nuclear receptors. These results suggest that the cerebrum toxicity caused by Cd was reduced by pretreatment with RES. © 2023 Society of Chemical Industry.
AbstractList Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood-brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which leads to lethal cerebral edema, intracellular accumulation and cellular dysfunction, remains to be illuminated with regard to the exact molecular mechanism of cerebral toxicity. Resveratrol (RES), present in the edible portions of numerous plants, is a simply acquirable and correspondingly less toxic natural compound with neuroprotective potential, which provides some theoretical bases for antagonizing Cd-induced cerebral toxicity. This work was executed to research the protective effects of RES against Cd-induced toxicity in chicken cerebrum. Markedly, these lesions were increased in the Cd group, which also exhibited a thinner cortex, reduced granule cells, vacuolar degeneration, and an enlarged medullary space in the cerebrum. Furthermore, Cd induced CYP450 enzyme metabolism disorders by disrupting the nuclear xenobiotic receptor response (NXRs), enabling the cerebrum to reduce the ability to metabolize exogenous substances, eventually leading to Cd accumulation. Meanwhile, accumulated Cd promoted oxidative damage and synergistically promoted the damage to neurons and glial cells. RES initiated NXRs (especially for aromatic receptor and pregnancy alkane X receptor), decreasing the expression of CYP450 genes, changing the content of CYP450, maintaining CYP450 enzyme normal activities, and exerting antagonistic action against the Cd-induced abnormal response of nuclear receptors. These results suggest that the cerebrum toxicity caused by Cd was reduced by pretreatment with RES. © 2023 Society of Chemical Industry.
BACKGROUND: Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood–brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which leads to lethal cerebral edema, intracellular accumulation and cellular dysfunction, remains to be illuminated with regard to the exact molecular mechanism of cerebral toxicity. Resveratrol (RES), present in the edible portions of numerous plants, is a simply acquirable and correspondingly less toxic natural compound with neuroprotective potential, which provides some theoretical bases for antagonizing Cd‐induced cerebral toxicity. RESULTS: This work was executed to research the protective effects of RES against Cd‐induced toxicity in chicken cerebrum. Markedly, these lesions were increased in the Cd group, which also exhibited a thinner cortex, reduced granule cells, vacuolar degeneration, and an enlarged medullary space in the cerebrum. Furthermore, Cd induced CYP450 enzyme metabolism disorders by disrupting the nuclear xenobiotic receptor response (NXRs), enabling the cerebrum to reduce the ability to metabolize exogenous substances, eventually leading to Cd accumulation. Meanwhile, accumulated Cd promoted oxidative damage and synergistically promoted the damage to neurons and glial cells. CONCLUSION: RES initiated NXRs (especially for aromatic receptor and pregnancy alkane X receptor), decreasing the expression of CYP450 genes, changing the content of CYP450, maintaining CYP450 enzyme normal activities, and exerting antagonistic action against the Cd‐induced abnormal response of nuclear receptors. These results suggest that the cerebrum toxicity caused by Cd was reduced by pretreatment with RES. © 2023 Society of Chemical Industry.
BACKGROUND Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood–brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which leads to lethal cerebral edema, intracellular accumulation and cellular dysfunction, remains to be illuminated with regard to the exact molecular mechanism of cerebral toxicity. Resveratrol (RES), present in the edible portions of numerous plants, is a simply acquirable and correspondingly less toxic natural compound with neuroprotective potential, which provides some theoretical bases for antagonizing Cd‐induced cerebral toxicity. RESULTS This work was executed to research the protective effects of RES against Cd‐induced toxicity in chicken cerebrum. Markedly, these lesions were increased in the Cd group, which also exhibited a thinner cortex, reduced granule cells, vacuolar degeneration, and an enlarged medullary space in the cerebrum. Furthermore, Cd induced CYP450 enzyme metabolism disorders by disrupting the nuclear xenobiotic receptor response (NXRs), enabling the cerebrum to reduce the ability to metabolize exogenous substances, eventually leading to Cd accumulation. Meanwhile, accumulated Cd promoted oxidative damage and synergistically promoted the damage to neurons and glial cells. CONCLUSION RES initiated NXRs (especially for aromatic receptor and pregnancy alkane X receptor), decreasing the expression of CYP450 genes, changing the content of CYP450, maintaining CYP450 enzyme normal activities, and exerting antagonistic action against the Cd‐induced abnormal response of nuclear receptors. These results suggest that the cerebrum toxicity caused by Cd was reduced by pretreatment with RES. © 2023 Society of Chemical Industry.
Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood-brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which leads to lethal cerebral edema, intracellular accumulation and cellular dysfunction, remains to be illuminated with regard to the exact molecular mechanism of cerebral toxicity. Resveratrol (RES), present in the edible portions of numerous plants, is a simply acquirable and correspondingly less toxic natural compound with neuroprotective potential, which provides some theoretical bases for antagonizing Cd-induced cerebral toxicity.BACKGROUNDCadmium (Cd), known as a vital contaminant in the environment, penetrates the blood-brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which leads to lethal cerebral edema, intracellular accumulation and cellular dysfunction, remains to be illuminated with regard to the exact molecular mechanism of cerebral toxicity. Resveratrol (RES), present in the edible portions of numerous plants, is a simply acquirable and correspondingly less toxic natural compound with neuroprotective potential, which provides some theoretical bases for antagonizing Cd-induced cerebral toxicity.This work was executed to research the protective effects of RES against Cd-induced toxicity in chicken cerebrum. Markedly, these lesions were increased in the Cd group, which also exhibited a thinner cortex, reduced granule cells, vacuolar degeneration, and an enlarged medullary space in the cerebrum. Furthermore, Cd induced CYP450 enzyme metabolism disorders by disrupting the nuclear xenobiotic receptor response (NXRs), enabling the cerebrum to reduce the ability to metabolize exogenous substances, eventually leading to Cd accumulation. Meanwhile, accumulated Cd promoted oxidative damage and synergistically promoted the damage to neurons and glial cells.RESULTSThis work was executed to research the protective effects of RES against Cd-induced toxicity in chicken cerebrum. Markedly, these lesions were increased in the Cd group, which also exhibited a thinner cortex, reduced granule cells, vacuolar degeneration, and an enlarged medullary space in the cerebrum. Furthermore, Cd induced CYP450 enzyme metabolism disorders by disrupting the nuclear xenobiotic receptor response (NXRs), enabling the cerebrum to reduce the ability to metabolize exogenous substances, eventually leading to Cd accumulation. Meanwhile, accumulated Cd promoted oxidative damage and synergistically promoted the damage to neurons and glial cells.RES initiated NXRs (especially for aromatic receptor and pregnancy alkane X receptor), decreasing the expression of CYP450 genes, changing the content of CYP450, maintaining CYP450 enzyme normal activities, and exerting antagonistic action against the Cd-induced abnormal response of nuclear receptors. These results suggest that the cerebrum toxicity caused by Cd was reduced by pretreatment with RES. © 2023 Society of Chemical Industry.CONCLUSIONRES initiated NXRs (especially for aromatic receptor and pregnancy alkane X receptor), decreasing the expression of CYP450 genes, changing the content of CYP450, maintaining CYP450 enzyme normal activities, and exerting antagonistic action against the Cd-induced abnormal response of nuclear receptors. These results suggest that the cerebrum toxicity caused by Cd was reduced by pretreatment with RES. © 2023 Society of Chemical Industry.
BACKGROUNDCadmium (Cd), known as a vital contaminant in the environment, penetrates the blood–brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which leads to lethal cerebral edema, intracellular accumulation and cellular dysfunction, remains to be illuminated with regard to the exact molecular mechanism of cerebral toxicity. Resveratrol (RES), present in the edible portions of numerous plants, is a simply acquirable and correspondingly less toxic natural compound with neuroprotective potential, which provides some theoretical bases for antagonizing Cd‐induced cerebral toxicity.RESULTSThis work was executed to research the protective effects of RES against Cd‐induced toxicity in chicken cerebrum. Markedly, these lesions were increased in the Cd group, which also exhibited a thinner cortex, reduced granule cells, vacuolar degeneration, and an enlarged medullary space in the cerebrum. Furthermore, Cd induced CYP450 enzyme metabolism disorders by disrupting the nuclear xenobiotic receptor response (NXRs), enabling the cerebrum to reduce the ability to metabolize exogenous substances, eventually leading to Cd accumulation. Meanwhile, accumulated Cd promoted oxidative damage and synergistically promoted the damage to neurons and glial cells.CONCLUSIONRES initiated NXRs (especially for aromatic receptor and pregnancy alkane X receptor), decreasing the expression of CYP450 genes, changing the content of CYP450, maintaining CYP450 enzyme normal activities, and exerting antagonistic action against the Cd‐induced abnormal response of nuclear receptors. These results suggest that the cerebrum toxicity caused by Cd was reduced by pretreatment with RES. © 2023 Society of Chemical Industry.
Author Li, Jin‐Long
Lv, Mei‐Wei
Zhang, Cong
Ge, Jing
Sun, Xiao‐Han
Li, Jin‐Yang
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Keywords cadmium
neurotoxicity
AHR/CAR/PXR pathway
CYP450
resveratrol
NXRs
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Notes Mei‐Wei Lv, Cong Zhang, Jing Ge these authors contributed equally to this study.
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PublicationCentury 2000
PublicationDate September 2023
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2023-Sep
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PublicationDateYYYYMMDD 2023-09-01
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  year: 2023
  text: September 2023
PublicationDecade 2020
PublicationPlace Chichester, UK
PublicationPlace_xml – name: Chichester, UK
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PublicationTitle Journal of the science of food and agriculture
PublicationTitleAlternate J Sci Food Agric
PublicationYear 2023
Publisher John Wiley & Sons, Ltd
John Wiley and Sons, Limited
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References 2018; 120
2012; 200
2022; 170
2019; 11
2018; 206
2021; 28
2018; 365
2020; 249
2021; 285
2020; 11
2019; 689
2020; 10
2014; 28
2013; 8
2012; 52
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2022; 242
2001; 299
2005; 141
2002; 141
2000; 57
2023; 135
2023; 134
2013; 96
2014; 14
2013; 273
2021; 153
2010; 193
2012; 25
2007; 21
2007; 23
2014; 56
2023; 71
2003; 42
2001; 98
2012; 146
2003; 138
2009; 20
2017; 2017
2021; 783
2021; 225
2021; 147
2021; 227
2020; 260
2018; 63
2014; 40
2018; 66
2022; 234
2016; 7
2010; 42
2009; 30
2005; 19
2021; 11
2021; 773
2015; 2015
2005; 207
2022; 13
2023; 312
1994; 15
2002; 71
2022; 11
2022; 227
2018; 98
2012; 89
2017; 226
2022; 105
2016; 68
2016; 23
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Snippet BACKGROUND Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood–brain barrier and accumulates in the cerebrum. Acute toxicosis...
Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood-brain barrier and accumulates in the cerebrum. Acute toxicosis of Cd, which...
BACKGROUNDCadmium (Cd), known as a vital contaminant in the environment, penetrates the blood–brain barrier and accumulates in the cerebrum. Acute toxicosis of...
BACKGROUND: Cadmium (Cd), known as a vital contaminant in the environment, penetrates the blood–brain barrier and accumulates in the cerebrum. Acute toxicosis...
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SubjectTerms agriculture
AHR/CAR/PXR pathway
Alkanes
Blood-brain barrier
Cadmium
Cadmium - metabolism
Cadmium - toxicity
Cerebrum
Cerebrum - metabolism
chickens
Contaminants
cortex
CYP450
Cytochrome
cytochrome P-450
Cytochrome P-450 Enzyme System - genetics
Cytochrome P-450 Enzyme System - metabolism
Cytochrome P-450 Enzyme System - pharmacology
Cytochrome P450
Cytochromes P450
Damage accumulation
Degeneration
Edema
Enzymes
Gene expression
Glial cells
Granule cells
Metabolism
Microsomes
Microsomes - metabolism
Molecular modelling
Neurodegeneration
Neuronal-glial interactions
Neuroprotection
neuroprotective effect
neurotoxicity
Nuclear receptors
NXRs
Oxidative Stress
poisoning
pregnancy
Receptors
Receptors, Cytoplasmic and Nuclear - metabolism
Resveratrol
Resveratrol - metabolism
Resveratrol - pharmacology
Toxicity
Toxicosis
vacuoles
xenobiotics
Title Resveratrol protects against cadmium‐induced cerebrum toxicity through modifications of the cytochrome P450 enzyme system in microsomes
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjsfa.12668
https://www.ncbi.nlm.nih.gov/pubmed/37115015
https://www.proquest.com/docview/2844101670
https://www.proquest.com/docview/2807922793
https://www.proquest.com/docview/2887605446
Volume 103
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