Functional aspects of oxidative phosphorylation and electron transport in cardiac mitochondria of copper-deficient rats

J. M. Matz; J. T. Saari; A. M. Bode

doi:10.1016/0955-2863(95)00146-8

Functional aspects of oxidative phosphorylation and electron transport in cardiac mitochondria of copper-deficient rats

J. M. Matz, J. T. Saari, A. M. Bode

Research output: Contribution to journal › Article › peer-review

15 Scopus citations

Abstract

Although dietary copper deficiency causes physiological, morphological, and biochemical abnormalities in cardiac mitochondria, the relationship observed between abnormalities of mitochondrial structure and function have been inconsistent in previous studies. The purpose of the present study was to re-evaluate the respiration rates of cardiac mitochondria from copper-deficient rats and to use several drugs that uncouple and inhibit mitochondrial respiration in order to clarify the mechanisms of mitochondrial dysfunction found in several laboratories. Copper deficiency reduced state 4 and state 3 cardiac mitochondrial respiration rates with all substrates tested. However, neither the ratio of ADP/oxygen consumed nor the acceptor control index was affected by copper deficiency. Cardiac mitochondria of copper-deficient rats showed a resistance to respiratory blockade by oligomycin and an increased ability to hydrolyze ATP in the presence of oligomycin compared with mitochondria of copper-adequate rats. This suggests that copper deficiency affects the function of the cardiac mitochondrial ATP synthase.

Original language	English (US)
Pages (from-to)	644-652
Number of pages	9
Journal	The Journal of Nutritional Biochemistry
Volume	6
Issue number	12
DOIs	https://doi.org/10.1016/0955-2863(95)00146-8
State	Published - Dec 1995
Externally published	Yes

Bibliographical note

Funding Information:
This work was supported in part by the USDA, ARS. Mention of a trademark or propriety product does not constitute a guarantee or warranty of the product by the US Department of Agriculture and does not imply its approval to the exclusion of other products that may also be suitable. This is a US government work. There are no restrictions on its use. The U.S. Department of Agriculture, Agricultural Research Service, Northern Plains Area, is an equal opportunity/affirmative action employer and all agency services are available without discrimination. We thank Jackie Keith and Gwen Schelkoph for their technical service and assistance .

Keywords

ATP synthase
electron transport
mitochondrial respiration
oxidative phosphorylation

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10.1016/0955-2863(95)00146-8

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title = "Functional aspects of oxidative phosphorylation and electron transport in cardiac mitochondria of copper-deficient rats",

abstract = "Although dietary copper deficiency causes physiological, morphological, and biochemical abnormalities in cardiac mitochondria, the relationship observed between abnormalities of mitochondrial structure and function have been inconsistent in previous studies. The purpose of the present study was to re-evaluate the respiration rates of cardiac mitochondria from copper-deficient rats and to use several drugs that uncouple and inhibit mitochondrial respiration in order to clarify the mechanisms of mitochondrial dysfunction found in several laboratories. Copper deficiency reduced state 4 and state 3 cardiac mitochondrial respiration rates with all substrates tested. However, neither the ratio of ADP/oxygen consumed nor the acceptor control index was affected by copper deficiency. Cardiac mitochondria of copper-deficient rats showed a resistance to respiratory blockade by oligomycin and an increased ability to hydrolyze ATP in the presence of oligomycin compared with mitochondria of copper-adequate rats. This suggests that copper deficiency affects the function of the cardiac mitochondrial ATP synthase.",

keywords = "ATP synthase, electron transport, mitochondrial respiration, oxidative phosphorylation",

author = "Matz, \{J. M.\} and Saari, \{J. T.\} and Bode, \{A. M.\}",

note = "Funding Information: This work was supported in part by the USDA, ARS. Mention of a trademark or propriety product does not constitute a guarantee or warranty of the product by the US Department of Agriculture and does not imply its approval to the exclusion of other products that may also be suitable. This is a US government work. There are no restrictions on its use. The U.S. Department of Agriculture, Agricultural Research Service, Northern Plains Area, is an equal opportunity/affirmative action employer and all agency services are available without discrimination. We thank Jackie Keith and Gwen Schelkoph for their technical service and assistance .",

year = "1995",

month = dec,

doi = "10.1016/0955-2863(95)00146-8",

language = "English (US)",

volume = "6",

pages = "644--652",

journal = "The Journal of Nutritional Biochemistry",

issn = "0955-2863",

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TY - JOUR

T1 - Functional aspects of oxidative phosphorylation and electron transport in cardiac mitochondria of copper-deficient rats

AU - Matz, J. M.

AU - Saari, J. T.

AU - Bode, A. M.

N1 - Funding Information: This work was supported in part by the USDA, ARS. Mention of a trademark or propriety product does not constitute a guarantee or warranty of the product by the US Department of Agriculture and does not imply its approval to the exclusion of other products that may also be suitable. This is a US government work. There are no restrictions on its use. The U.S. Department of Agriculture, Agricultural Research Service, Northern Plains Area, is an equal opportunity/affirmative action employer and all agency services are available without discrimination. We thank Jackie Keith and Gwen Schelkoph for their technical service and assistance .

PY - 1995/12

Y1 - 1995/12

N2 - Although dietary copper deficiency causes physiological, morphological, and biochemical abnormalities in cardiac mitochondria, the relationship observed between abnormalities of mitochondrial structure and function have been inconsistent in previous studies. The purpose of the present study was to re-evaluate the respiration rates of cardiac mitochondria from copper-deficient rats and to use several drugs that uncouple and inhibit mitochondrial respiration in order to clarify the mechanisms of mitochondrial dysfunction found in several laboratories. Copper deficiency reduced state 4 and state 3 cardiac mitochondrial respiration rates with all substrates tested. However, neither the ratio of ADP/oxygen consumed nor the acceptor control index was affected by copper deficiency. Cardiac mitochondria of copper-deficient rats showed a resistance to respiratory blockade by oligomycin and an increased ability to hydrolyze ATP in the presence of oligomycin compared with mitochondria of copper-adequate rats. This suggests that copper deficiency affects the function of the cardiac mitochondrial ATP synthase.

AB - Although dietary copper deficiency causes physiological, morphological, and biochemical abnormalities in cardiac mitochondria, the relationship observed between abnormalities of mitochondrial structure and function have been inconsistent in previous studies. The purpose of the present study was to re-evaluate the respiration rates of cardiac mitochondria from copper-deficient rats and to use several drugs that uncouple and inhibit mitochondrial respiration in order to clarify the mechanisms of mitochondrial dysfunction found in several laboratories. Copper deficiency reduced state 4 and state 3 cardiac mitochondrial respiration rates with all substrates tested. However, neither the ratio of ADP/oxygen consumed nor the acceptor control index was affected by copper deficiency. Cardiac mitochondria of copper-deficient rats showed a resistance to respiratory blockade by oligomycin and an increased ability to hydrolyze ATP in the presence of oligomycin compared with mitochondria of copper-adequate rats. This suggests that copper deficiency affects the function of the cardiac mitochondrial ATP synthase.

KW - ATP synthase

KW - electron transport

KW - mitochondrial respiration

KW - oxidative phosphorylation

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U2 - 10.1016/0955-2863(95)00146-8

DO - 10.1016/0955-2863(95)00146-8

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AN - SCOPUS:0029176035

SN - 0955-2863

VL - 6

SP - 644

EP - 652

JO - The Journal of Nutritional Biochemistry

JF - The Journal of Nutritional Biochemistry

IS - 12

ER -

Functional aspects of oxidative phosphorylation and electron transport in cardiac mitochondria of copper-deficient rats

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