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暴露于低温环境下的新生雏鸡不同组织中的氧化损伤。

Oxidative damage in different tissues of neonatal chicks exposed to low environmental temperature.

作者信息

Mujahid Ahmad, Furuse Mitsuhiro

机构信息

Laboratory of Advanced Animal and Marine Bioresources, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan.

出版信息

Comp Biochem Physiol A Mol Integr Physiol. 2009 Apr;152(4):604-8. doi: 10.1016/j.cbpa.2009.01.011.

Abstract

Maintenance of body temperature in a cold environment is crucial for survival in homeotherms. However, we have previously reported that on exposure to low environmental temperature, neonatal chicks (Gallus gallus) show hypothermia, decreased behavioral activity, and absence of gene transcript enhancement of putative thermogenic proteins, as well as no change in mitochondrial substrate oxidation enzymes. Various metabolic abnormalities and/or tissue damage may also decline the thermogenic capacity of low-temperature-exposed neonatal chicks. Therefore, to investigate oxidative damage in low-temperature-exposed (20 degrees C for 12 h) neonatal chicks, we studied lipid peroxidation when compared to the control chicks kept at thermoneutral temperature (30 degrees C). Malondialdehyde (MDA), was measured in plasma, brain, heart, liver and skeletal muscle (pectoralis superficialis and gastrocnemius). Weight gain and feed consumption did not change when chicks were exposed to low-temperature as compared to that of control chicks. On low-temperature exposure, body temperature was significantly decreased and plasma non-esterified fatty acid level was 1.3-fold higher than that of control chicks. In low-temperature exposed chicks, brain and heart MDA levels were 2.1- and 1.2-fold higher, respectively, than that of control chicks. This increase in MDA levels was not observed in plasma, liver and muscle of low-temperature-exposed chicks. In conclusion, there is evidence of increased lipid peroxidation in brain and heart of neonatal chicks exposed to low-temperature. We hypothesize that this oxidative damage in brain and heart may contribute to the impaired physiological, behavioral and thermoregulatory responses that potentiate the sensitivity to cold exposure.

摘要

在寒冷环境中维持体温对于恒温动物的生存至关重要。然而,我们之前报道过,新生雏鸡(原鸡)暴露于低温环境时会出现体温过低、行为活动减少、假定产热蛋白的基因转录增强缺失,以及线粒体底物氧化酶无变化。各种代谢异常和/或组织损伤也可能降低低温暴露新生雏鸡的产热能力。因此,为了研究低温暴露(20摄氏度,12小时)的新生雏鸡的氧化损伤,我们将其与处于热中性温度(30摄氏度)的对照雏鸡相比,研究了脂质过氧化情况。在血浆、脑、心脏、肝脏和骨骼肌(胸浅肌和腓肠肌)中测量了丙二醛(MDA)。与对照雏鸡相比,雏鸡暴露于低温时体重增加和采食量没有变化。低温暴露时,体温显著降低,血浆非酯化脂肪酸水平比对照雏鸡高1.3倍。在低温暴露的雏鸡中,脑和心脏的MDA水平分别比对照雏鸡高2.1倍和1.2倍。在低温暴露雏鸡的血浆、肝脏和肌肉中未观察到MDA水平的这种升高。总之,有证据表明低温暴露的新生雏鸡脑和心脏中的脂质过氧化增加。我们推测,脑和心脏中的这种氧化损伤可能导致生理、行为和体温调节反应受损,从而增强对寒冷暴露的敏感性。

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