Effects of reproduction on immuno-suppression and oxidative damage, and hence support or otherwise for their roles as mechanisms underpinning life history trade-offs, are tissue and assay dependent
Effects of reproduction on immuno-suppression and oxidative damage, and hence support or otherwise for their roles as mechanisms underpinning life history trade-offs, are tissue and assay dependent
复制标题
DOI：
10.1242/jeb.092049
复制
发表时间：
2013-11
影响因子：
2.8
通讯作者：
Dengbao Yang;Yanchao Xu;Dehua Wang;J. Speakman
中科院分区：
文献类型：
--
作者：
Dengbao Yang;Yanchao Xu;Dehua Wang;J. Speakman
生活史参数似乎相互抵消，但涉及的生理机制尚不清楚。一种假设是，由于选择性资源分配，免疫功能和氧化应激保护等潜在的能量消耗过程可能在生殖尝试中受到损害。较低的温度也会增加能量消耗，因此当动物被迫在寒冷环境中繁殖时，分配决策可能会更加明显。在这里，我们通过实验测试了蒙古沙鼠（Meriones unguiculatus）在不同环境温度下的繁殖是否与氧化应激升高和免疫功能抑制有关。使用多种不同的免疫功能和氧化应激标志物，我们发现，与非生殖沙鼠相比，泌乳沙鼠的某些免疫功能指标（血清杀菌能力和胸腺大小）明显受到抑制，而一些氧化保护指标（血清超氧化物歧化酶（SOD）活性和谷胱甘肽过氧化物酶（GPx）活性）也降低，氧化损伤指标（血清蛋白羰基）升高。这些变化符合选择性资源分配预测。然而，与非生殖沙鼠相比，泌乳沙鼠的植物血凝素反应和血清总免疫球蛋白（IgG）并未受到抑制，其他氧化损伤标志物[肝脏中的丙二醛（MDA） （TBARS）和蛋白质羰基]实际上更低，这与肝脏中SOD活性和总抗氧化能力水平的增加相一致。后一种变化与基于资源分配的期望相反。此外，其他保护措施（肝脏中的GPx水平和血清和肝脏中的蛋白硫醇）和损伤[血清中的MDA (TBARS)]与生殖状态无关。环境温差对这些模式没有影响。总的来说，我们的研究结果表明，生殖对免疫抑制和氧化损伤的推断影响，从而支持或不支持支撑生活史权衡的特定生理机制，严重依赖于所使用的确切标记和组织。这可能是因为在繁殖过程中，个体选择性地将保护分配给某些关键组织，而牺牲了对其他组织的保护。
SUMMARY Life history parameters appear to be traded off against each other, but the physiological mechanisms involved remain unclear. One hypothesis is that potentially energetically costly processes such as immune function and protection from oxidative stress may be compromised during reproductive attempts because of selective resource allocation. Lower temperatures also impose energy costs, and hence allocation decisions might be more pronounced when animals are forced to reproduce in the cold. Here, we experimentally tested whether reproduction at different ambient temperatures was associated with elevated oxidative stress and suppressed immune function in Mongolian gerbils (Meriones unguiculatus). Using a variety of different markers for both immune function and oxidative stress, we found that some measures of immune function (serum bactericidal capacity and size of the thymus) were significantly suppressed, while some measures of oxidative protection [serum superoxide dismutase (SOD) activity and glutathione peroxidase (GPx) activity] were also reduced, and a marker of oxidative damage (protein carbonyls in serum) was increased in lactating compared with non-reproductive gerbils. These changes were in line with the selective resource allocation predictions. However, the phytohaemagglutinin response and serum total immunoglobulin (IgG) were not suppressed, and other markers of oxidative damage [malondialdehyde (MDA) (TBARS) and protein carbonyls in the liver] were actually lower in lactating compared with non-reproductive gerbils, consistent with increased levels of SOD activity and total antioxidant capacity in the liver. These latter changes were opposite of the expectations based on resource allocation. Furthermore, other measures of protection (GPx levels in the liver and protein thiols in both serum and liver) and damage [MDA (TBARS) in serum] were unrelated to reproductive status. Ambient temperature differences did not impact on these patterns. Collectively, our results indicated that the inferred effects of reproduction on immunosuppression and oxidative damage, and hence support or otherwise for particular physiological mechanisms that underpin life history trade-offs, are critically dependent on the exact markers and tissues used. This may be because during reproduction individuals selectively allocate protection to some key tissues, but sacrifice protection of others.