Association between heat stress and oxidative stress in poultry; mitochondrial dysfunction and dietary interventions with phytochemicals.
Association between heat stress and oxidative stress in poultry; mitochondrial dysfunction and dietary interventions with phytochemicals.
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DOI：
10.1186/s40104-016-0097-5
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发表时间：
2016
影响因子：
7
通讯作者：
De Smet S
中科院分区：
文献类型：
--
作者：
Akbarian A;Michiels J;Degroote J;Majdeddin M;Golian A;De Smet S
几十年来，人们对高温作为家禽的一种应激源进行了广泛的研究；它影响着世界范围内的家禽生产，并对福祉和生产产生重大影响。最近，热应激在诱导氧化应激中的作用引起了人们的极大兴趣。氧化应激的定义是活性物种的存在超过了动物细胞的现有抗氧化能力。活性物质可以修饰几个生物细胞大分子，并可以干扰细胞信号通路。此外，在过去的十年中，人们对使用各种天然饲料传递的植物化学物质的兴趣与日俱增，这些化学物质对家禽具有潜在的抗氧化性能。有鉴于此，本文综述了(1)热应激引发线粒体超氧阴离子自由基产生并进展为氧化应激的机制，(2)阐明这一病理生理机制依赖于热应激的强度和持续时间，(3)提出了缓解线粒体功能障碍的不同营养策略，尤其是抗氧化性植物化学物质。热暴露引起的氧化应激可见于身体的各个部位；然而，线粒体功能障碍是氧化应激的基础。在急性热应激的初期，线粒体底物氧化和电子传输链活性增加，导致超氧化物产生过多。在急性热应激的后期，禽解偶联蛋白的下调加剧了氧化应激状况，导致线粒体功能障碍和组织损伤。通常情况下，抗氧化酶活性会被上调。然而，慢性热应激导致线粒体代谢氧化能力下降，禽解偶联蛋白上调，抗氧化酶活性模式明显改变，抗氧化剂储备耗尽。一些植物化学物质，如各种类型的类黄酮类和相关化合物，被证明对慢性热应激家禽有益，但对非热应激家禽效果较差或无效。这支持了这样的观点，即抗氧化植物化学物质在具有挑战性的条件下具有潜力。虽然我们对热应激和氧化应激之间的关系的理解已经取得了实质性的进展，但植物化学物质可以缓解氧化应激的方法还很少被探索。本文的在线版本(doi：10.1186/s40104-0160097-5)包含补充材料，授权用户可以使用。
Heat as a stressor of poultry has been studied extensively for many decades; it affects poultry production on a worldwide basis and has significant impact on well-being and production. More recently, the involvement of heat stress in inducing oxidative stress has received much interest. Oxidative stress is defined as the presence of reactive species in excess of the available antioxidant capacity of animal cells. Reactive species can modify several biologically cellular macromolecules and can interfere with cell signaling pathways. Furthermore, during the last decade, there has been an ever-increasing interest in the use of a wide array of natural feed-delivered phytochemicals that have potential antioxidant properties for poultry. In light of this, the current review aims to (1) summarize the mechanisms through which heat stress triggers excessive superoxide radical production in the mitochondrion and progresses into oxidative stress, (2) illustrate that this pathophysiology is dependent on the intensity and duration of heat stress, (3) present different nutritional strategies for mitigation of mitochondrial dysfunction, with particular focus on antioxidant phytochemicals. Oxidative stress that occurs with heat exposure can be manifest in all parts of the body; however, mitochondrial dysfunction underlies oxidative stress. In the initial phase of acute heat stress, mitochondrial substrate oxidation and electron transport chain activity are increased resulting in excessive superoxide production. During the later stage of acute heat stress, down-regulation of avian uncoupling protein worsens the oxidative stress situation causing mitochondrial dysfunction and tissue damage. Typically, antioxidant enzyme activities are upregulated. Chronic heat stress, however, leads to downsizing of mitochondrial metabolic oxidative capacity, up-regulation of avian uncoupling protein, a clear alteration in the pattern of antioxidant enzyme activities, and depletion of antioxidant reserves. Some phytochemicals, such as various types of flavonoids and related compounds, were shown to be beneficial in chronic heat-stressed poultry, but were less or not effective in non-heat-stressed counterparts. This supports the contention that antioxidant phytochemicals have potential under challenging conditions. Though substantial progress has been made in our understanding of the association between heat stress and oxidative stress, the means by which phytochemicals can alleviate oxidative stress have been sparsely explored. The online version of this article (doi:10.1186/s40104-016-0097-5) contains supplementary material, which is available to authorized users.