首页> 外文期刊>Biochemistry (Moscow). Supplement, Series A. Membrane and cell biology >Amaranth Seed Oil: Effect of Oral Administrationon Energetic Functions of Rat Liver Mitochondria Activated with Adrenaline
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Amaranth Seed Oil: Effect of Oral Administrationon Energetic Functions of Rat Liver Mitochondria Activated with Adrenaline

机译:菜籽油:口服对肾上腺素激活的大鼠肝线粒体能量功能的影响

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Respiration parameters of liver mitochondria (MCh) in rats fed with amaranth seed oil for 3 weekshave been evaluated. Thirty minutes before decapitation, adrenaline was injected intraperitoneally at a low dose(350 gg/kg body weight) to both control and experimental animals. It was shown that in animals that wereinjected with adrenaline and did not receive oil, the rate of phosphorylating respiration increased by 32% andphosphorylation time decreased by 22% upon oxidation of succinate; upon oxidation of α-ketoglutarate in thepresence of the succinate dehydrogenase inhibitor malonate, phosphorylating respiration was activated by 23%.The respiration of MCh upon oxidation of succinate + glutamate and α-ketoglutarate in the absence of malonatewas not affected by adrenaline. The intake of oil markedly activated almost all parameters of mitochondrial res-piration in experimental rats upon oxidation of all above-listed substrates in both coupled and uncoupled MCh.However, phosphorylation time was close to the control value (upon oxidation of succinate) or increased (uponoxidation of α-ketoglutarate in the presence and absence of malonate). The injection of adrenaline to animalsreceiving oil did not affect the oil-activated respiration of MCh oxidizing the substrates used; however, phos-phorylation time in all groups of animals decreased. Ca~(2+)capacity of MCh in rats receiving amaranth oil didnot change. Thus, our data show that feeding of rats with amaranth oil activates mitochondrial respiration andprevents MCh hyperactivation induced by adrenaline.
机译:评价了喂食a菜籽油3周的大鼠肝线粒体(MCh)的呼吸参数。断头前30分钟,以低剂量(350 gg / kg体重)腹膜内向对照动物和实验动物注射肾上腺素。结果表明,在注射了肾上腺素但不加油的动物中,琥珀酸的氧化使磷酸化呼吸速率增加了32%,磷酸化时间减少了22%。在琥珀酸脱氢酶抑制剂丙二酸存在下氧化α-酮戊二酸时,磷酸化呼吸作用被激活23%。在没有丙二酸存在的情况下,琥珀酸+谷氨酸和α-酮戊二酸氧化后的MCh呼吸作用不受肾上腺素的影响。在耦合和非耦合的MCh中,所有以上列出的底物都被氧化后,油的摄入显着激活了实验大鼠中几乎所有的线粒体再海盗参数,但是磷酸化时间接近于控制值(琥珀酸氧化时)或增加(在存在和不存在丙二酸酯的情况下,α-酮戊二酸的过氧化)。向接受油的动物注射肾上腺素不会影响MCh氧化所用底物的油激活呼吸作用。然而,所有动物组的磷酸化时间都减少了。 a菜油大鼠体内MCh的Ca〜(2+)容量没有变化。因此,我们的数据表明,用mar菜油喂养大鼠可激活线粒体呼吸并防止肾上腺素引起的MCh过度活化。

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