Hydroxyl Radical Generation and Membrane Fluidity of Erythrocytes Treated with Lipopolysaccharide

Hino, Yuji; Kumashiro, Ryukichi; Sata, Michio; Nishi, Juichi; Ogura, Ryohei; Tanikawa, Kyuichi

doi:10.3109/10715769309056s177

Cited by 7 publications

(2 citation statements)

References 10 publications

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“…Although the precise chemical structure of AcA has not been identified, the main structure is believed to consist of a hydrophobic lipid portion and a hydrophilic saccharide portion, and is thus easily incorporated into the lipid bilayer. LPS is incorporated into the lipid bilayer of cell membranes via its lipid A portion and reduces membrane fluidity by preventing the motion of phospholipid acyl chains (Jacobs, 1984;Hino et al, 1993). The present results showed that AcA increased the membrane fluidity of endothelial cells.…”

Section: Discussionmentioning

confidence: 46%

Effects of Actinomyces Amphiphile on the Fluidity of Endothelial Cells: A Spin Label Study

Hamada

1996

J Dent Res

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Actinomyces amphiphile (AcA) is an amphipathic molecule produced by Actinomyces viscosus that exhibits several biological activities. The effect of AcA on the fluidity and permeability of the plasma membrane in human umbilical vein endothelial cells was analyzed by a spin label method with 5- and 16-stearic acid nitroxide labels (SAL). These labels help to visualize the fluidity at the shallow (5-SAL) and deep (16-SAL) portions of the lipid bilayer. Cells were incubated with and without AcA (control) at 37 degrees C for 6 hours, and membrane fluidity was periodically measured. Another spin label, 4-(N, N-dimethyl-N-hexadecyl) ammonium-2, 2, 6, 6-tetramethyl-piperidine-1-oxyliodine (CAT-16), was also used to assess the physical state of the cell surface. The order parameter of 5-SAL was significantly lower in the cells incubated with AcA than in control cells after the six-hour incubation. The motion parameter of 16-SAL was significantly lower in AcA-treated cells than in controls after 4 and 6 hours of incubation. These findings indicated that the AcA increased the fluidity. There were no significant differences between the AcA-treated and control cells incubated for only 2 hours. In addition, there were no differences in CAT-16 measurements between AcA-treated and control cells. The release of endoplasmic lactate dehydrogenase (LDH) into the medium tended to increase in the AcA-treated vs. the control cells. LDH release increased in both a dose- and time-dependent manner, indicating that AcA increased the permeability of plasma membranes. These findings suggest that AcA alters the biophysical properties of the plasma membranes of endothelial cells, affecting membrane function.

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Section: Discussionmentioning

confidence: 46%

Effects of Actinomyces Amphiphile on the Fluidity of Endothelial Cells: A Spin Label Study

Hamada

1996

J Dent Res

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“…These results indicate that OH suppresses 45Ca2~influx by inhibiting L-type VDCCs. Based on the previous report that OH shows various effects on membrane functions and intracellular biochemical events (Varani et a!., 1985;Davies et al, 1987;Solar et a!., 1990;Hino et a!., 1993;Pieper et a!., 1993), it is assumed that the inhibition of L-type VDCCs is one of the biochemical actions of~OH on membrane functions. However, at present the mechanisms for such inhibitory actions of OH on L-type VDCCs are not clear.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms for Facilitation of Nitric Oxide‐Evoked [³H]GABA Release by Removal of Hydroxyl Radical

Ohkuma¹,

Katsura²,

Hibino

et al. 1998

Journal of Neurochemistry

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We have investigated the mechanisms for enhancement of nitric oxide (NO)‐evoked γ‐[3H]aminobutyric acid ([3H]GABA) release from mouse cerebro‐cortical neurons by hydroxyl radical (•OH) scavengers. •OH scavengers, such as N,N′‐dimethylthiourea (DMTU), uric acid, and mannitol, dose‐dependently facilitated NO‐evoked [3H]GABA release evoked by NO liberated from S‐nitroso‐N‐acetylpenicillamine. Ionomycin‐evoked [3H]GABA release, which was significantly inhibited by hemoglobin and an NO synthase, NG‐methyl‐l‐arginine, was also enhanced by DMTU. These results indicate that GABA release evoked by both endogenous and exogenous NO is facilitated by •OH scavengers. These enhancing actions of •OH scavengers were completely abolished by Ca2+ removal from incubation buffer and by an l‐type voltage‐dependent Ca2+ channel (VDCC) inhibitor, nifedipine, whereas each •OH scavenger showed no effects on [3H]GABA release in the absence of NO. Inhibitors for P/Q‐ and N‐type VDCCs had no effects on the enhancement. NO‐induced 45Ca2+ influx was also dose‐dependently enhanced by •OH scavengers, although 45Ca2+ influx was not altered by •OH scavengers in the absence of NO. Nifedipine abolished this enhancement of the NO‐induced 45Ca2+ influx by •OH scavengers. These results indicate that the removal of •OH by its scavengers facilitates the NO‐evoked [3H]GABA release dependent on Ca2+ and that this enhancement is due to the increase in Ca2+ influx via L‐type VDCCs.

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Hydroxyl radical scavengers enhance nitric oxide-evoked acetylcholine release from mouse cerebral cortical neurons

Ohkuma

Katsura

Chen

et al. 1995

Molecular Brain Research

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Hydroxyl Radical Generation and Membrane Fluidity of Erythrocytes Treated with Lipopolysaccharide

Cited by 7 publications

References 10 publications

Effects of Actinomyces Amphiphile on the Fluidity of Endothelial Cells: A Spin Label Study

Effects of Actinomyces Amphiphile on the Fluidity of Endothelial Cells: A Spin Label Study

Mechanisms for Facilitation of Nitric Oxide‐Evoked [³H]GABA Release by Removal of Hydroxyl Radical

Hydroxyl radical scavengers enhance nitric oxide-evoked acetylcholine release from mouse cerebral cortical neurons

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Hydroxyl Radical Generation and Membrane Fluidity of Erythrocytes Treated with Lipopolysaccharide

Cited by 7 publications

References 10 publications

Effects of Actinomyces Amphiphile on the Fluidity of Endothelial Cells: A Spin Label Study

Effects of Actinomyces Amphiphile on the Fluidity of Endothelial Cells: A Spin Label Study

Mechanisms for Facilitation of Nitric Oxide‐Evoked [3H]GABA Release by Removal of Hydroxyl Radical

Hydroxyl radical scavengers enhance nitric oxide-evoked acetylcholine release from mouse cerebral cortical neurons

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Mechanisms for Facilitation of Nitric Oxide‐Evoked [³H]GABA Release by Removal of Hydroxyl Radical