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Studies on cardiac energy supply, mitochondrial respiration, ATP synthase and cytochrome c oxidase in copper-deficient and/or dimethyl sulfoxide-treated rats from biochemical and molecular biological aspects.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Studies on cardiac energy supply, mitochondrial respiration, ATP synthase and cytochrome c oxidase in copper-deficient and/or dimethyl sulfoxide-treated rats from biochemical and molecular biological aspects./
作者:	Chao, Chen-Jui.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 1993,
面頁冊數:	209 p.
附註:	Source: Dissertations Abstracts International, Volume: 55-03, Section: B.
Contained By:	Dissertations Abstracts International55-03B.
標題:	Nutrition. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9325470
ISBN:	9798208446157

Studies on cardiac energy supply, mitochondrial respiration, ATP synthase and cytochrome c oxidase in copper-deficient and/or dimethyl sulfoxide-treated rats from biochemical and molecular biological aspects.
Chao, Chen-Jui.

Studies on cardiac energy supply, mitochondrial respiration, ATP synthase and cytochrome c oxidase in copper-deficient and/or dimethyl sulfoxide-treated rats from biochemical and molecular biological aspects. - Ann Arbor : ProQuest Dissertations & Theses, 1993 - 209 p.

Source: Dissertations Abstracts International, Volume: 55-03, Section: B.

Thesis (Ph.D.)--The Ohio State University, 1993.

This item must not be added to any third party search indexes.

Cardiac hypertrophy is a common sign of copper deficiency in rodents. Potential changes in energy metabolism of hearts from copper-deficient rats were investigated. Cardiac nucleotide and phosphocreatine pools and mitochondrial respiration were studied in male Long-Evans rats fed either copper-adequate or -deficient diets for 5 weeks from weaning. Results suggested that cardiac ATP levels were maintained in copper-deficient rats despite lower cytochrome c oxidase activity, respiratory control ratio and oxygen consumption rate. Previous studies suggested that the copper-deficient rat heart appears to have decreased levels of the $\\delta$ subunit of ATP synthase and the nuclear-encoded subunits of cytochrome c oxidase. Since copper-deficient rat hearts have compromised mitochondrial morphology and membranes, another goal of the study was to determine if decreased peptide levels were secondary to the pathology or due to a lack of copper per se. Blocking of much of the pathological damage by administrating the antioxidant dimethyl sulfoxide (DMSO) in conjunction with feeding a copper-deficient diet was used to determine if the altered peptide levels were due to the lack of copper. Rats were randomly assigned to six groups: ad libitum copper-adequate and -deficient, DMSO-treated copper-adequate and -deficient, and copper-adequate and -deficient pair-fed to the corresponding DMSO groups. As expected, DMSO administration reduced the presence of compromised heart morphology in copper-deficient rats. The $\\delta$ subunit of ATP synthase and cytochrome c oxidase nuclear-encoded subunits IV and V were depressed in all groups fed the copper-deficient diet regardless of DMSO administration or pair versus ad libitum feeding. These results strongly suggested the altered peptides were not due to compromised heart pathology. Furthermore, Northern blotting analysis of oligonucleotide probes to quantify mRNA's of cytochrome c oxidase subunits II and IV revealed no difference by treatments, suggesting the decreased subunit IV levels were not due to any effect of copper at the transcriptional level. These data suggest that post-translational/transcriptional aspects may be responsible for the altered enzyme peptide subunits in the copper-deficient rat heart.

ISBN: 9798208446157Subjects--Topical Terms:

517777
Nutrition.
Subjects--Index Terms:

dimethyl sulfoxide

Studies on cardiac energy supply, mitochondrial respiration, ATP synthase and cytochrome c oxidase in copper-deficient and/or dimethyl sulfoxide-treated rats from biochemical and molecular biological aspects.
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500 $a Publisher info.: Dissertation/Thesis.
500 $a Advisor: Medeiros, Denis M.
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506 $a This item must not be added to any third party search indexes.
506 $a This item must not be sold to any third party vendors.
520 $a Cardiac hypertrophy is a common sign of copper deficiency in rodents. Potential changes in energy metabolism of hearts from copper-deficient rats were investigated. Cardiac nucleotide and phosphocreatine pools and mitochondrial respiration were studied in male Long-Evans rats fed either copper-adequate or -deficient diets for 5 weeks from weaning. Results suggested that cardiac ATP levels were maintained in copper-deficient rats despite lower cytochrome c oxidase activity, respiratory control ratio and oxygen consumption rate. Previous studies suggested that the copper-deficient rat heart appears to have decreased levels of the $\\delta$ subunit of ATP synthase and the nuclear-encoded subunits of cytochrome c oxidase. Since copper-deficient rat hearts have compromised mitochondrial morphology and membranes, another goal of the study was to determine if decreased peptide levels were secondary to the pathology or due to a lack of copper per se. Blocking of much of the pathological damage by administrating the antioxidant dimethyl sulfoxide (DMSO) in conjunction with feeding a copper-deficient diet was used to determine if the altered peptide levels were due to the lack of copper. Rats were randomly assigned to six groups: ad libitum copper-adequate and -deficient, DMSO-treated copper-adequate and -deficient, and copper-adequate and -deficient pair-fed to the corresponding DMSO groups. As expected, DMSO administration reduced the presence of compromised heart morphology in copper-deficient rats. The $\\delta$ subunit of ATP synthase and cytochrome c oxidase nuclear-encoded subunits IV and V were depressed in all groups fed the copper-deficient diet regardless of DMSO administration or pair versus ad libitum feeding. These results strongly suggested the altered peptides were not due to compromised heart pathology. Furthermore, Northern blotting analysis of oligonucleotide probes to quantify mRNA's of cytochrome c oxidase subunits II and IV revealed no difference by treatments, suggesting the decreased subunit IV levels were not due to any effect of copper at the transcriptional level. These data suggest that post-translational/transcriptional aspects may be responsible for the altered enzyme peptide subunits in the copper-deficient rat heart.
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