Contribution of Lipid Dynamics on the Inhibition of Bovine Brain Synaptosomal Na+-K+-ATPase Activity Induced by 4-Hydroxy-2-nonenal

Kadoya, Akinori; Miyake, Hiromi; Ohyashiki, Takao

doi:10.1248/bpb.26.787

Cited by 22 publications

(10 citation statements)

References 34 publications

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“…38) We have recently reported that the Na ϩ /K ϩ ATPase activity of bovine synaptosomal and reconstituted membranes is markedly inhibited by interaction of the membrane constituents with 4-hydroxy-2-nonenal. 39,40) These findings also pose the possibility that the breakdown products of lipid hydroperoxides are related to the onset mechanism of Al toxicity.…”

Section: Fig 6 Effects Of Nac and Other Antioxidants On Ros Productionmentioning

confidence: 90%

Glutathione Depletion Promotes Aluminum-Mediated Cell Death of PC12 Cells

Satoh

Okada

Takadera

et al. 2005

Biological & Pharmaceutical Bulletin

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Section: Fig 6 Effects Of Nac and Other Antioxidants On Ros Productionmentioning

confidence: 90%

Glutathione Depletion Promotes Aluminum-Mediated Cell Death of PC12 Cells

Satoh

Okada

Takadera

et al. 2005

Biological & Pharmaceutical Bulletin

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“…HNE can lead to an alteration in the lipid dynamics of membranes, 11,12) which can affect the function of transmembrane proteins. We have recently reported that the inhibition of bovine cerebral synaptosomal Na ϩ -K ϩ -ATPase activity associated with modification of the membranes by HNE is closely related to the decreased lipid fluidity at the lipid/water interface on the membrane surface.…”

mentioning

confidence: 99%

Increase in Molecular Rigidity of the Protein Conformation of Brain Na+-K+-ATPase by Modification with 4-Hydroxy-2-nonenal

Miyake

Kadoya

Ohyashiki

2003

Biological & Pharmaceutical Bulletin

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The effect of lipid peroxidation product 4-hydroxy-2-nonenal (HNE) on the protein conformation of porcine cerebral cortex Na(+)-K(+)-ATPase was examined in term of the intrinsic tryptophanyl fluorescence measurement. Treatment of ATPase with HNE resulted in a decrease in the fluorescence intensity and an increase in the fluorescence anisotropy in a concentration-dependent manner. The difference in the fluorescence intensity and fluorescence anisotropy observed between the control and HNE-modified ATPase completely disappeared after treatment of the protein with guanidine hydrochloride (1 M). These results suggest that HNE-modification of the Na(+)-K(+)-ATPase induces alterations in the conformation of the enzyme molecule. This interpretation was further supported by a decrease in fluorescence quenching efficiency with acrylamide and sulfhydryl (SH) content. The decrease in quenching efficiency suggests that the proximity of the quencher molecule to the fluorophores located in the enzyme is suppressed. Modification of the enzyme with N-ethylmaleimide (NEM) also resulted in a decrease in quenching efficiency with the loss of SH groups. Furthermore, a good relationship between the SH content and these fluorescence parameters (fluorescence anisotropy and quenching efficiency) were observed. On the other hand, treatment of the Na(+)-K(+)-ATPase with other aldehydes such as malondialdehyde (MDA), 1-hexanal and nonanal did not affect either the quenching efficiency or SH content. Based on these results, the possibility of alterations in the physical properties of the Na(+)-K(+)-ATPase associated with modification by HNE has been discussed.

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“…,K ? -ATPase has been observed following exposure to oxygen radical generating system or to lipid peroxidation end products like 4-hydroxy-2-nonenal (Kovachich and Mishra 1981;Mishra et al 1989;Lehotsky et al 1999;Miyake et al 2003;Kadoya et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Dietary supplementation with N-acetylcysteine, α-tocopherol and α-lipoic acid prevents age related decline in Na+,K+-ATPase activity and associated peroxidative damage in rat brain synaptosomes

et al. 2008

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This study has shown that in aged rat brain (22-24 months) crude synaptosomes in comparison to that in young animals (4-6 months), a striking decrease in the activity of Na(+),K(+)-ATPase occurs along with decreased K (m) and V (max) but without any change in enzyme content as seen by immunoblotting. This is associated with an accumulation of peroxidative damage products in aged brain. When rats are given antioxidant supplementation in the diet with a combination of N-acetylcysteine, alpha-tocopherol and alpha-lipoic acid daily from 18 months onwards and sacrificed at 22-24 months for experimentation, the age associated decrease of Na(+),K(+)-ATPase activity, alterations of its kinetic parameters and accumulation of peroxidative damage products in brain synaptosomes are prevented nearly completely. Because of the critical importance of Na(+),K(+)-ATPase in neuronal functions, the results of this study may be of potential implications in controlling age-related functional deficits of the brain.

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Contribution of Lipid Dynamics on the Inhibition of Bovine Brain Synaptosomal Na+-K+-ATPase Activity Induced by 4-Hydroxy-2-nonenal

Cited by 22 publications

References 34 publications

Glutathione Depletion Promotes Aluminum-Mediated Cell Death of PC12 Cells

Glutathione Depletion Promotes Aluminum-Mediated Cell Death of PC12 Cells

Increase in Molecular Rigidity of the Protein Conformation of Brain Na+-K+-ATPase by Modification with 4-Hydroxy-2-nonenal

Dietary supplementation with N-acetylcysteine, α-tocopherol and α-lipoic acid prevents age related decline in Na+,K+-ATPase activity and associated peroxidative damage in rat brain synaptosomes

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