Kuczynski Beth, Reo Nicholas V
Department of Biochemistry and Molecular Biology, Wright State University School of Medicine, WSU Magnetic Resonance Laboratory, Cox Institute, Dayton, OH 45429, USA.
Neurochem Res. 2006 May;31(5):639-56. doi: 10.1007/s11064-006-9061-7. Epub 2006 May 24.
The antioxidant capabilities of phosphatidylethanolamine plasmalogen (PlsEtn), in vivo, against lipid peroxidation were investigated via acute phosphine (PH(3)) administration in rats. Oxidative stress was assessed from measures of malondialdehyde and various enzyme activities, while NMR analyses of lipid and aqueous tissue extracts provided metabolic information in cerebellum, brainstem, and cortex. Brainstem had the highest basal [PlsEtn], and showed only moderate PH(3)-induced oxidative damage with no loss of ATP. The lowest basal [PlsEtn] was observed in cortex, where PH(3) caused a 51% decrease in [ATP]. The largest oxidative effect occurred in cerebellum, but [ATP] was unaffected. Myo-inositol+ethanolamine pretreatment attenuated all PH(3) effects. Specifically, the pretreatment attenuated the ATP decrease in cortex, and elevated brain [PlsEtn] in the cerebellum, nearly abolishing the cerebellar oxidative effects. Our data suggest a high basal [PlsEtn], or the capacity to synthesize new ethanolamine lipids (particularly PlsEtn) may protect against PH(3) toxicity.
通过对大鼠急性给予磷化氢(PH₃),研究了磷脂酰乙醇胺缩醛磷脂(PlsEtn)在体内对抗脂质过氧化的抗氧化能力。通过丙二醛和各种酶活性的测定来评估氧化应激,而对脂质和水性组织提取物的核磁共振分析提供了小脑、脑干和皮质的代谢信息。脑干的基础[PlsEtn]最高,并且仅显示出中度的PH₃诱导的氧化损伤,ATP没有损失。在皮质中观察到最低的基础[PlsEtn],其中PH₃导致[ATP]下降51%。最大的氧化效应发生在小脑中,但[ATP]未受影响。肌醇+乙醇胺预处理减弱了所有PH₃的效应。具体而言,预处理减轻了皮质中ATP的下降,并提高了小脑中脑[PlsEtn],几乎消除了小脑的氧化效应。我们的数据表明,高基础[PlsEtn]或合成新的乙醇胺脂质(特别是PlsEtn)的能力可能预防PH₃毒性。