Walters Jessica L H, Anderson Amanda L, Martins da Silva Sarah J, Aitken R John, De Iuliis Geoffry N, Sutherland Jessie M, Nixon Brett, Bromfield Elizabeth G
Priority Research Centre for Reproductive Science, Schools of Biomedical Science & Pharmacy and Environmental & Life Sciences, The University of Newcastle, Callaghan, NSW 2308, Australia.
Hunter Medical Research Institute, Pregnancy and Reproduction Program, New Lambton Heights, NSW 2305, Australia.
Antioxidants (Basel). 2020 Dec 31;10(1):43. doi: 10.3390/antiox10010043.
A prevalent cause of sperm dysfunction in male infertility patients is the overproduction of reactive oxygen species, an attendant increase in lipid peroxidation and the production of cytotoxic reactive carbonyl species such as 4-hydroxynonenal. Our previous studies have implicated arachidonate 15-lipoxygenase (ALOX15) in the production of 4-hydroxynonenal in developing germ cells. Here, we have aimed to develop a further mechanistic understanding of the lipoxygenase-lipid peroxidation pathway in human spermatozoa. Through pharmacological inhibition studies, we identified a protective role for phospholipase enzymes in the liberation of peroxidised polyunsaturated fatty acids from the human sperm membrane. Our results also revealed that arachidonic acid, linoleic acid and docosahexanoic acid are key polyunsaturated fatty acid substrates for ALOX15. Upon examination of ALOX15 in the spermatozoa of infertile patients compared to their normozoospermic counterparts, we observed significantly elevated levels of ALOX15 protein abundance in the infertile population and an increase in 4-hydroxynonenal adducts. Collectively, these data confirm the involvement of ALOX15 in the oxidative stress cascade of human spermatozoa and support the notion that increased ALOX15 abundance in sperm cells may accentuate membrane lipid peroxidation and cellular dysfunction, ultimately contributing to male infertility.
男性不育患者精子功能障碍的一个普遍原因是活性氧的过量产生、脂质过氧化作用随之增加以及细胞毒性反应性羰基化合物(如4-羟基壬烯醛)的产生。我们之前的研究表明,花生四烯酸15-脂氧合酶(ALOX15)在发育中的生殖细胞中4-羟基壬烯醛的产生过程中起作用。在此,我们旨在进一步从机制上理解人类精子中的脂氧合酶-脂质过氧化途径。通过药理学抑制研究,我们确定了磷脂酶在从人类精子膜中释放过氧化多不饱和脂肪酸方面的保护作用。我们的结果还表明,花生四烯酸、亚油酸和二十二碳六烯酸是ALOX15的关键多不饱和脂肪酸底物。在检查不育患者与正常精子患者的精子中的ALOX15时,我们观察到不育人群中ALOX15蛋白丰度显著升高,且4-羟基壬烯醛加合物增加。总体而言,这些数据证实了ALOX15参与人类精子的氧化应激级联反应,并支持这样一种观点,即精子细胞中ALOX15丰度增加可能会加剧膜脂质过氧化和细胞功能障碍,最终导致男性不育。