In insects, prolonged exposure to unseasonably low temperatures can lead to detrimental physiological effects known as chill injury. Changes to active and passive transport across epithelia during chilling likely drive the collapse of ion gradients, metabolic imbalance and potentially oxidative stress. In the alfalfa leafcutting bee, Megachile rotundata transcriptomic evidence provides support for these responses at the level of gene expression, but variable expression profiles between life stages in M. rotundata indicate that different mechanisms could be responsible for repairing and protecting against chill injuries across development. Herein, we test the hypotheses that 1) chill injury leads to oxidative stress and damage in insects and 2) exposure to a fluctuating thermal regime (FTR) promotes an increased oxidative stress response leading to a decrease in damage by reactive oxygen species. We measured the expression of transcripts with products known to have antioxidant properties in overwintering prepupae as well as total antioxidant capacity and lipid peroxidation during both extended overwintering in prepupae and low temperature stress during pupal development. We observed differential gene expression for the antioxidant glutathione peroxidase and several transcripts with putative antioxidant properties including vitellogenin, apolipoprotein D, glutathione S-transferase, and nuclear protein 1. However, the expression of transcripts coding for other enzymatic antioxidants did not change between treatments. Neither life stage varied in their capacity to cope with an induced oxidative stress after FTR exposure and we did not observe evidence of lipid peroxidation in chill injured (STR) prepupae. These results did not support our initial hypotheses and indicate that oxidative-stress-induced damage is neither a causal factor or symptom of chill injury.

中文翻译：

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不断变化的热态可以防止寒害，但不会改变苜蓿切叶蜂Megachile rotundata的氧化应激模式。

在昆虫中，长时间暴露在不合季节的低温下会导致有害的生理效应，称为寒害。冷却期间跨上皮的主动和被动运输的变化可能导致离子梯度的崩溃，代谢失衡和潜在的氧化应激。在苜蓿切叶蜂中，Megachile rotundata转录组证据为基因表达水平上的这些应答提供了支持，但在Ro.data的生命阶段之间的可变表达谱表明，不同的机制可能负责修复和预防整个发育过程中的寒害。在这里 我们测试了以下假设：1）寒冷伤害导致昆虫氧化应激和损害，以及2）暴露于波动的热态（FTR）会促进氧化应激反应的增加，从而导致活性氧对伤害的减少。我们测量了已知在越冬prepupae中具有抗氧化特性的产品的转录本的表达，以及在越过prepupae的越冬期间以及在小total发育过程中的低温胁迫下的总抗氧化能力和脂质过氧化作用。我们观察到抗氧化剂谷胱甘肽过氧化物酶的基因表达差异，以及具有推定抗氧化特性的几个转录本，包括卵黄蛋白原，载脂蛋白D，谷胱甘肽S-转移酶和核蛋白1。但是，处理之间，编码其他酶促抗氧化剂的转录本表达没有变化。在暴露于FTR后，这两个生命阶段都没有改变应对氧化应激的能力，而且我们也没有观察到冷伤（STR）足p中脂质过氧化的证据。这些结果不支持我们最初的假设，并表明氧化应激诱导的损伤既不是寒意伤害的因果也不是症状。