兔在短期高温下的脑脂质。

K Domańska-Janik, Z Dabrowiecki, W Gordon-Majszak, J Strosznajder
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引用次数: 0

摘要

将家兔在40℃高温下加热3小时,脑组织磷脂含量没有变化,而游离脂肪酸含量比对照水平增加了约73%。热疗也诱导脂肪酸过氧化过程的抑制。脂肪酸过氧化的最后产物,硫代巴比妥酸反应物质,在高温下显著减少,而该途径的第一中间体,共轭双键的水平保持不变。同时,脂溶性抗氧化剂水平显著降低。游离脂肪酸、丙二醛和脂溶性抗氧化剂的含量在恢复后3小时内恢复到控制水平。在热疗后立即和3小时检查的动物组中,神经节苷脂的含量比对照组高10-20%。神经节苷脂特异性酶,神经氨酸酶和唾液基转移酶,都指向内源性脂质底物,被热疗激活,表明在热疗过程中刺激神经节苷脂的转换。短期高温引起的脂质改变可能影响神经元膜的理化性质。
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Rabbit brain lipids during short-term hyperthermia.

Rabbits were subjected to 3 h of hyperthermia at 40 degrees C. The phospholipid content of the brain was unchanged, whereas the free fatty acids increased by about 73% over control levels. Hyperthermia also induced inhibition of fatty acid peroxidation processes. The last products of fatty acid peroxidation, the thiobarbituric acid reactive substances, diminished significantly during hyperthermia, whereas the level of the first intermediate of this pathway, the conjugated double bonds, remained unchanged. Simultaneously, the levels of lipid-soluble antioxidants decreased significantly. The content of free fatty acids, malondialdehyde, and lipid-soluble anti-oxidant returned toward control levels during 3 h of recovery. The content of gangliosides was 10-20% above control values in the groups of animals examined immediately and 3 h after hyperthermia. The ganglioside-specific enzymes, neuraminidase and sialyltransferase, both directed toward endogenous lipid substrates, were activated by hyperthermia, suggesting the stimulation of turnover of the gangliosides during the course of hyperthermia. Lipid alterations resulting from short-term hyperthermia may influence the physicochemical properties of neuronal membranes.

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