During outdoor large-scale cultivation, Haematococcus pluvialis cells, especially at the green motile stage, are frequently exposed to chilling stress in winter. However, the physiological responses and adaptation mechanisms to chilling in H. pluvialis have not been characterized. In order to better understand the chilling tolerance mechanisms of H. pluvialis in the green motile stage, the responses of photosynthetic characteristics and photoprotective mechanisms to chilling were investigated. Chilling stress significantly decreased the activities of key enzymes (ribulose-1,5-bisphosphate carboxylase/oxygenase and NADP glyceraldehyde-3-phosphate dehydrogenase) in photosynthetic carbon assimilation, which would cause the accumulation of excess reducing equivalents and an imbalance of light absorption and energy utilization, leading to more severe photoinhibition. After chilling treatment, there was no induction of cyclic electron flow, non-photochemical quenching, fluorescence emission, or catalase, indicating these factors do not protect H. pluvialis from photoinhibition. However, chilling significantly enhanced the activities of antioxidant enzymes (superoxide dismutase, ascorbate peroxidase, dehydroascorbate reductase, and glutathione reductase), which efficiently dissipated excess electrons generated by photosynthetic linear electron flow (LEF). The malate-oxaloacetate shuttle was activated and the mitochondrial alternative oxidase (AOX) pathway was significantly up-regulated after chilling, indicating the transport of excess reducing equivalents generated by photosynthetic LEF to cytosol and mitochondria and oxidization by the AOX pathway, the mitochondrial non-phosphorylating pathway. As a result, the LEF was not inhibited by negative feedback and the H. pluvialis cells were well protected under chilling stress in the light, with no change in the effective quantum yield of PSII (Φ_PSII) and the yield of non-regulated energy dissipation of PSII (Φ_NO). The results indicate that antioxidant enzymes and the mitochondrial AOX pathway play important roles in protecting H. pluvialis at the green motile stage against chilling stress.

在室外大规模栽培期间，红血球菌细胞，特别是在绿色运动阶段，在冬天经常暴露于寒冷胁迫下。但是，尚未鉴定出对湿润嗜盐杆菌寒冷的生理反应和适应机制。为了更好地理解的耐冷性机制H.生红球藻在绿色运动阶段，研究了光合作用和光保护机制对低温的响应。低温胁迫显着降低了光合作用碳同化过程中关键酶（核糖-1,5-双磷酸羧化酶/加氧酶和NADP甘油醛-3-磷酸脱氢酶）的活性，这将导致过量的还原当量的积累以及光吸收和吸收的不平衡。能源利用，导致更严重的光​​抑制作用。冷却处理后，没有诱导循环电子流，非光化学猝灭，荧光发射或过氧化氢酶，表明这些因素不能保护幽门螺杆菌从光抑制。但是，冷却显着增强了抗氧化酶（超氧化物歧化酶，抗坏血酸过氧化物酶，脱氢抗坏血酸还原酶和谷胱甘肽还原酶）的活性，从而有效地消散了由光合线性电子流（LEF）产生的过量电子。冷却后，苹果酸-草酰乙酸盐转运蛋白被激活，线粒体替代氧化酶（AOX）途径被显着上调，表明光合作用LEF产生的过量还原当量向细胞质和线粒体的转运以及通过AOX途径（线粒体非-磷酸化途径。其结果是，在LEF不是由负反馈和抑制H.生红球藻细胞下的光低温胁迫，与PSII的有效量子产率（Φ无变化被很好的保护_PSII）和PSII的非管制能量耗散（Φ的收率_NO）。结果表明在保护抗氧化酶和线粒体AOX途径中发挥重要作用H.生红球藻在对低温胁迫的绿色运动型阶段。