Department of Electron Microscopy and Environmental Toxicology, National Institute of Pathology, New Delhi, India.
Am J Reprod Immunol. 2012 Dec;68(6):486-90. doi: 10.1111/aji.12023. Epub 2012 Sep 17.
There is a possibility that mitochondrial respiration defects may contribute to asthenozoospermia.
Immunocytochemical detection was used to localize succinic dehydrogenase (SDH) in the head and mid-piece of spermatozoa by fluorescent microscope.
The study revealed dispersed SDH activity in the semen of asthenozoospermic subjects in comparison with control semen samples. While the stain intensity varied from cell to cell in controls as well as in patients, it was predominantly localized within mid-piece of spermatozoa in healthy individuals. In contrast, in semen of infertile male, the diffused and dispersed SDH immunoreactivity was observed in head as well as in mid-piece region of spermatozoa.
Dispersed expression of mitochondrial SDH in head and mid-piece of spermatozoa of asthenozoospermia subjects indicates mitochondrial damage because of metabolic or genetic factors, affecting energy production and leading to disturbed sperm motility, which could be pathologically significant. Detailed mitochondrial SDH immunolocalization studies are warranted to establish a role of deranged tricarboxylic acid cycle in causation of male infertility.
线粒体呼吸缺陷可能导致弱精症。
通过荧光显微镜，使用免疫细胞化学检测法定位精子头部和中段的琥珀酸脱氢酶（SDH）。
与对照组精液相比，研究显示弱精症患者的精液中 SDH 活性呈弥散分布。虽然对照组和患者组的染色强度在细胞间存在差异，但在健康个体中，SDH 主要定位于精子中段。相比之下，在不育男性的精液中，SDH 的弥散和分散免疫反应性既存在于精子头部，也存在于中段。
弱精症患者精子头部和中段的线粒体 SDH 呈弥散表达，表明代谢或遗传因素导致线粒体损伤，影响能量产生并导致精子运动障碍，这可能具有病理意义。需要进行详细的线粒体 SDH 免疫定位研究，以确定三羧酸循环紊乱在男性不育症中的作用。
