Heat stress reduces cow milk yield and results in a significant economic loss for the dairy industry. During lactation, heat stress lowers milk production by 25 to 40% with half of the decrease in milk synthesis resulting from the reduced feed intake. In vitro studies indicate that primary bovine mammary epithelial cells display greater rates of programmed cell death when exposed to high ambient temperatures, which may lead to a decrease in the total number of mammary epithelial cells in the mammary gland, partially explaining the lower milk production of lactating cows under heat stress. The function of mammary cells is also altered by heat stress. In response to heat stress, mammary cells display higher gene expression of heat shock proteins, indicating a need for cytoprotection from protein aggregation and degradation. Further, heat stress results in increased gene expression without altering protein expression of mammary epithelial cell junction proteins, and does not substantially influence the integrity of mammary epithelium. These data suggest that the mammary gland strives to maintain cell-to-cell junction integrity by synthesizing more proteins to compensate for protein losses induced by heat stress. During the dry period, heat stress negatively affects mammary gland development by reducing mammary cell proliferation before parturition, resulting in a dramatic decrease in milk production in the subsequent lactation. In addition to mammary growth, the mammary gland of the heat-stressed dry cow has reduced protein expression of autophagic proteins in the early dry period, suggesting heat stress influences mammary involution. Emerging evidence also indicates that heifers born to cows that experience late-gestation heat stress have lower milk yield during their first lactation, implying that the maternal environment may alter mammary gland development of the offspring. It is not clear if this is due to a direct epigenetic modification of prenatal mammary gland development by maternal heat stress. More research is needed to elucidate the effect of heat stress on mammary gland development and function.

热应激会降低牛奶产量，并给乳品行业造成重大的经济损失。泌乳期间，热应激会使牛奶的产量降低25％至40％，而牛奶合成的一半减少是由于采食量减少所致。体外研究表明，暴露于高环境温度下，原代牛乳腺上皮细胞显示出更高的程序性细胞死亡率，这可能导致乳腺中乳腺上皮细胞总数减少，部分解释了牛乳产量降低的原因。在热应激下哺乳的奶牛。乳细胞的功能也会因热应激而改变。响应热应激，乳腺细胞显示出热休克蛋白的更高基因表达，表明需要保护细胞免受蛋白聚集和降解。进一步，热应激导致基因表达增加而不改变乳腺上皮细胞连接蛋白的蛋白质表达，并且基本上不影响乳腺上皮的完整性。这些数据表明，乳腺通过合成更多的蛋白质来补偿由热应激引起的蛋白质损失，努力保持细胞间连接的完整性。在干燥期，热应激会通过降低分娩前乳腺细胞的增殖而对乳腺的发育产生负面影响，从而导致随后泌乳期乳汁产量的急剧下降。除乳腺生长外，热应激的干奶牛的乳腺在干燥初期也降低了自噬蛋白的蛋白质表达，这表明热应激会影响乳腺退化。越来越多的证据还表明，经历后期妊娠热应激的母牛所生的小母牛在第一次泌乳期间的牛奶产量较低，这意味着母体环境可能会改变后代的乳腺发育。尚不清楚这是否是由于产妇热应激对产前乳腺发育的直接表观遗传修饰。需要更多的研究来阐明热应激对乳腺发育和功能的影响。