Bis(2-chloroethoxy)methane-Induced Mitochondrial and Myofibrillar Damage: Short-Term Time-Course Study.
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| Title: | Bis(2-chloroethoxy)methane-Induced Mitochondrial and Myofibrillar Damage: Short-Term Time-Course Study. |
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| Authors: | Dunnick, June1 dunnickj@niehs.nih.gov, Johnson, JoAnne2, Horton, John2, Nyska, Abraham2 |
| Source: | Toxicological Sciences. Sep2004, Vol. 81 Issue 1, p243-252. 10p. |
| Subjects: | Time study, Mitochondria, Transdermal medication, Sarcoplasmic reticulum, Toxicological interactions, Necrosis, Thiodiglycol, Methane, Physiology |
| Abstract: | Cardiotoxicity induced by 2-, 3-, 5-, and 12-day dermal administration of 400 and 600 mg/kg/day of bis(2-chloroethoxy)methane to F344/N male and female rats was characterized. The severity and incidence of lesions were similar among males and females and in all three regions of the heart examined (atrium, ventricle, interventricular septum). Damage induced by bis(2-chloroethoxy)methane consisted of time-related development of myofiber vacuolation, necrosis, mononuclear-cell infiltration, fibrosis, and atrial thrombosis. Changes were pronounced at day 2, increased in severity at day 3, appeared to decrease at day 5, and resolved by study-day 16 that corresponded to 12 dosings. Ultrastructural analysis of 2- and 5-day 600 mg/kg/day-treated females elucidated the primary site of damage, the mitochondrion, and two types of vacuolation, one that formed as damaged mitochondria became devoid of cristae and their bounding double membranes became reduced to singleness, and the other manifested as distention of the sarcoplasmic reticulum. After the initial damage induced by bis(2-chloroethoxy)methane, or its metabolite, thiodiglycolic acid, protective mechanisms within the heart were apparently initiated, enabling it to cope with the continued exposure to the toxicant while eliminating some damaged myofibers. [ABSTRACT FROM AUTHOR] |
| Copyright of Toxicological Sciences is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Engineering Source |
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| Header | DbId: egs DbLabel: Engineering Source An: 20606111 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: Bis(2-chloroethoxy)methane-Induced Mitochondrial and Myofibrillar Damage: Short-Term Time-Course Study. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Dunnick%2C+June%22">Dunnick, June</searchLink><relatesTo>1</relatesTo><i> dunnickj@niehs.nih.gov</i><br /><searchLink fieldCode="AR" term="%22Johnson%2C+JoAnne%22">Johnson, JoAnne</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Horton%2C+John%22">Horton, John</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Nyska%2C+Abraham%22">Nyska, Abraham</searchLink><relatesTo>2</relatesTo> – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22Toxicological+Sciences%22">Toxicological Sciences</searchLink>. Sep2004, Vol. 81 Issue 1, p243-252. 10p. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22Time+study%22">Time study</searchLink><br /><searchLink fieldCode="DE" term="%22Mitochondria%22">Mitochondria</searchLink><br /><searchLink fieldCode="DE" term="%22Transdermal+medication%22">Transdermal medication</searchLink><br /><searchLink fieldCode="DE" term="%22Sarcoplasmic+reticulum%22">Sarcoplasmic reticulum</searchLink><br /><searchLink fieldCode="DE" term="%22Toxicological+interactions%22">Toxicological interactions</searchLink><br /><searchLink fieldCode="DE" term="%22Necrosis%22">Necrosis</searchLink><br /><searchLink fieldCode="DE" term="%22Thiodiglycol%22">Thiodiglycol</searchLink><br /><searchLink fieldCode="DE" term="%22Methane%22">Methane</searchLink><br /><searchLink fieldCode="DE" term="%22Physiology%22">Physiology</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Cardiotoxicity induced by 2-, 3-, 5-, and 12-day dermal administration of 400 and 600 mg/kg/day of bis(2-chloroethoxy)methane to F344/N male and female rats was characterized. The severity and incidence of lesions were similar among males and females and in all three regions of the heart examined (atrium, ventricle, interventricular septum). Damage induced by bis(2-chloroethoxy)methane consisted of time-related development of myofiber vacuolation, necrosis, mononuclear-cell infiltration, fibrosis, and atrial thrombosis. Changes were pronounced at day 2, increased in severity at day 3, appeared to decrease at day 5, and resolved by study-day 16 that corresponded to 12 dosings. Ultrastructural analysis of 2- and 5-day 600 mg/kg/day-treated females elucidated the primary site of damage, the mitochondrion, and two types of vacuolation, one that formed as damaged mitochondria became devoid of cristae and their bounding double membranes became reduced to singleness, and the other manifested as distention of the sarcoplasmic reticulum. After the initial damage induced by bis(2-chloroethoxy)methane, or its metabolite, thiodiglycolic acid, protective mechanisms within the heart were apparently initiated, enabling it to cope with the continued exposure to the toxicant while eliminating some damaged myofibers. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of Toxicological Sciences is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1093/toxsci/kfh194 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 10 StartPage: 243 Subjects: – SubjectFull: Time study Type: general – SubjectFull: Mitochondria Type: general – SubjectFull: Transdermal medication Type: general – SubjectFull: Sarcoplasmic reticulum Type: general – SubjectFull: Toxicological interactions Type: general – SubjectFull: Necrosis Type: general – SubjectFull: Thiodiglycol Type: general – SubjectFull: Methane Type: general – SubjectFull: Physiology Type: general Titles: – TitleFull: Bis(2-chloroethoxy)methane-Induced Mitochondrial and Myofibrillar Damage: Short-Term Time-Course Study. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Dunnick, June – PersonEntity: Name: NameFull: Johnson, JoAnne – PersonEntity: Name: NameFull: Horton, John – PersonEntity: Name: NameFull: Nyska, Abraham IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 09 Text: Sep2004 Type: published Y: 2004 Identifiers: – Type: issn-print Value: 10966080 Numbering: – Type: volume Value: 81 – Type: issue Value: 1 Titles: – TitleFull: Toxicological Sciences Type: main |
| ResultId | 1 |
