Effect of sodium and potassium ions on mitochondrial oxidative phosphorylation. Studies with arsenate

Sandoval, F.; Gómez‐Puyou, Armando; Tuena, M.; Chávez, Edmundo; Peña, Antonio

doi:10.1021/bi00805a031

Cited by 19 publications

(4 citation statements)

References 19 publications

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“…Rates of exchange in the absence of exogenous ATP were less than 5% of those in the presence of ATP and were similar among different diet treatments. ATP/P32P]PI exchange rates found here are similar to those previously reported for rat liver mitochondria (Sandoval et al, 1970).…”

Section: Resultssupporting

confidence: 92%

Dynamic modulation of mitochondrial membrane physical properties and ATPase activity by diet lipid

Innis¹,

Clandinin²

1981

Biochemical Journal

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A longitudinal cross-over feeding design was used to investigate the relationship of dietary lipid composition to the membrane lipid environment and activity of mitochondrial ATPase in vivo. Rats were fed a polyunsaturated fatty-acid-rich oil (soya-bean oil) for 12 days, crossed-over to a monounsaturated fatty-acid-rich oil (rapeseed oil) for the next 11 days, then returned to soya-bean oil for 11 more days. Additional rats were fed either soya-bean oil or rapeseed oil throughout. Rats fed rapeseed oil had lower rates of ATPase-catalysed ATP/[32P]Pi exchange than rats fed soya-bean oil. Arrhenius plots showed higher transition temperature (Tt) and activation energy (Ea) for rats fed rapeseed oil. Switching from soya-bean oil to rapeseed oil was dynamically followed by changes in the thermotropic and kinetic properties of the mitochondrial ATPase exchange reaction. Returning to soya-bean oil reversed these changes. The rapid and reversible modulation of Tt caused by a change of the type of fat ingested suggests that membrane physicochemical properties are not under rigid intrinsic control but are continually modified by the profile of exogenously derived fatty acids. The studies suggest that in vivo the activity of mitochondrial ATPase is in part determined by dietary lipid via its influence on the microenvironment of the enzyme. The rapidity and ready reversibility of changes observed for this subcellular-membrane-bound enzyme suggest that dietary fatty-acid balance may be an important determinant of other membrane functions in the body.

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Section: Resultssupporting

confidence: 92%

Dynamic modulation of mitochondrial membrane physical properties and ATPase activity by diet lipid

Innis¹,

Clandinin²

1981

Biochemical Journal

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“…These particles are morphologically and biochemically simpler than intact mitochondria or digitonin particles which possess an Asi-induced ATPase. Possibly some of the effects of As, on these more complex systems reflect other energy-linked events such as ion movement, as suggested by Sandoval et al (1970) and Kagawa and Kagawa (1969). Possibly As, (or Pi) acts in conjunction with ADP at a respiration control site.…”

Section: Discussionmentioning

confidence: 97%

Inhibition of mitochondrial energy-linked functions by arsenate. Evidence for a nonhydrolytic mode of inhibitor action

Mitchell¹,

Chang²,

Huang³

et al. 1971

Biochemistry

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“…Findings in the present study, including increases in brain ATPase activities and decreased brain ATP concentration, would be in keeping with impaired oxidative phosphorylation. Arsenate has been shown to stimulate ATPase activity in vitro [34]. However, in liver there appeared to be an increase in the concentration of hepatic ATP in all arsenic-treated groups; the reason for this was uncertain but possibly may have reflected an initial compensatory response.…”

Section: Discussionmentioning

confidence: 88%

Effects of Arsenate on Growth and Physiology in Mallard Ducklings

Camardese

Hoffman

LeCaptain

et al. 1990

Environ Toxicol Chem

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Arsenic (As) has been found at elevated concentrations in irrigation drainwater and in aquatic plants utilized by waterfowl. Mallard (Anus phtyrhynchos) ducklings received an untreated diet (controls) or diets containing 30, 100 or 300 ppm As added as sodium arsenate. After 10 weeks blood and tissue samples were collected for biochemical and histological examination. Arsenic accumulated significantly in brain and liver of ducklings fed 100 or 300 ppm but did not result in histopathological lesions. The 300-ppm dietary As concentration decreased overall growth (weight gain) in males, whereas all concentrations of As decreased overall growth and rate of growth in females. Food consumption was less during the first three weeks in the 300-ppm group and during the second week for the 100-ppm group compared to controls. Plasma sorbitol dehydrogenase activity and plasma glucose concentration were higher in the 300-ppm group compared to controls. Plasma triglyceride concentration increased in all As-treated groups. Brain ATP was lower in the 300-ppm group and sodium/potassium-dependent ATPase activity was higher in the 30-and 100-ppm groups. Hepatic glutathione peroxidase activity was lower in the 300-ppm group and malondialdehyde lower in all treatment groups. All treatment levels caused elevation in hepatic glutathione and ATP concentrations. These findings, in combination with altered duckling behavior (increased resting time), suggest that concentrations of As that have been found in aquatic plants (up to 430 ppm dry weight) could adversely affect normal duckling development.

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Effect of sodium and potassium ions on mitochondrial oxidative phosphorylation. Studies with arsenate

Cited by 19 publications

References 19 publications

Dynamic modulation of mitochondrial membrane physical properties and ATPase activity by diet lipid

Dynamic modulation of mitochondrial membrane physical properties and ATPase activity by diet lipid

Inhibition of mitochondrial energy-linked functions by arsenate. Evidence for a nonhydrolytic mode of inhibitor action

Effects of Arsenate on Growth and Physiology in Mallard Ducklings

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