Blackmore P F, Eisoldt S
Department of Physiological Sciences, Eastern Virginia Medical School, P.O. Box 1980, Norfolk, VA 23501, USA.
Mol Hum Reprod. 1999 Jun;5(6):498-506. doi: 10.1093/molehr/5.6.498.
The neoglycoproteins alpha-D-mannose-bovine serum albumin (mannose-BSA) and N-acetyl-alpha-D-glucosamine-BSA (glucNAc-BSA) were shown to rapidly increase intracellular free calcium ([Ca2+]i) in human spermatozoa. The increase in [Ca2+]i induced by these neoglycoproteins accounts for the known ability of these compounds to induce the acrosome reaction in human spermatozoa. Our data support the hypothesis that mannose-BSA, but not progesterone, activates T-type Ca2+ channels in human spermatozoa for the following reasons: (i) the capacity of mannose-BSA to increase [Ca2+]i was inhibited by the specific T-type Ca2+ channel blocker mibefradil (IC50 = 10(-6) mol/l) while progesterone was not inhibited by 10(-5) M mibefradil; (ii) the effect of mannose-BSA to elevate [Ca2+]i was inhibited more potently by Ni2+ (IC50 = 0.1 mmol/l) than Cd2+ (IC50 = 0.5 mmol/l), whereas the effect of progesterone to elevate [Ca2+]i was inhibited equally by Ni2+ and Cd2+ (IC50 = 0.25 mmol/l); (iii) the effects of mannose-BSA and progesterone to increase [Ca2+]i were greater than additive. These data support the idea that mannose-BSA and progesterone were activating distinct Ca2+ channels, one of which was a T-type Ca2+ channel activated by mannose-BSA whereas the Ca2+ channel that was activated by progesterone has yet to be defined at the molecular level.
新糖蛋白α-D-甘露糖-牛血清白蛋白（甘露糖-BSA）和N-乙酰-α-D-葡糖胺-BSA（葡糖胺-BSA）已被证明能迅速增加人类精子细胞内的游离钙（[Ca2+]i）。这些新糖蛋白诱导的[Ca2+]i增加解释了这些化合物诱导人类精子顶体反应的已知能力。我们的数据支持以下假设：甘露糖-BSA而非孕酮激活人类精子中的T型Ca2+通道，原因如下：（i）特异性T型Ca2+通道阻滞剂米贝地尔（IC50 = 10(-6) mol/l）抑制了甘露糖-BSA增加[Ca2+]i的能力，而10(-5) M米贝地尔对孕酮没有抑制作用；（ii）Ni2+（IC50 = 0.1 mmol/l）比Cd2+（IC50 = 0.5 mmol/l）更有效地抑制了甘露糖-BSA升高[Ca2+]i的作用，而Ni2+和Cd2+（IC50 = 0.25 mmol/l）对孕酮升高[Ca2+]i的作用抑制程度相同；（iii）甘露糖-BSA和孕酮增加[Ca2+]i的作用大于两者相加的效果。这些数据支持这样一种观点，即甘露糖-BSA和孕酮激活了不同的Ca2+通道，其中之一是由甘露糖-BSA激活的T型Ca2+通道，而由孕酮激活的Ca2+通道在分子水平上尚未明确。
