A neutral sphingomyelinase in spermatozoal plasma membranes

Hinkovska, V.T.; Petkova, Diana; Koumanov, Kamen

doi:10.1139/o87-067

Cited by 22 publications

(8 citation statements)

References 2 publications

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“…This possibility deserves more attention, but the present evidence does not make a compelling case for it. A neutral SMase has been reported in ram sperm plasma membranes [55], but capacitation does not decrease the sphingomyelin content of guinea pig or boar sperm [56][57][58].…”

Section: Discussionmentioning

confidence: 99%

Sphingomyelin Modulates Capacitation of Human Sperm In Vitro1

Cross

2000

Biology of Reproduction

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Ejaculated mammalian sperm must mature (capacitate) before they can undergo acrosomal exocytosis and fertilize an egg. Loss of sperm sterols is an early step in capacitation. Because sphingomyelin slows cholesterol efflux from other cells, the role of sphingomyelin in capacitation was tested. Human sperm were exposed to sphingomyelinase and then incubated for as long as 24 h. The ability of sperm to acrosome-react in response to progesterone was tested to measure capacitation. Sphingomyelinase-treated sperm became responsive to progesterone approximately 10 h earlier than control sperm. Sphingomyelinase also increased spontaneous acrosomal exocytosis. The effects of sphingomyelinase were accompanied by accelerated losses of the inhibitory sterols, cholesterol and desmosterol. To test whether sphingomyelinase-generated ceramide might promote capacitation, sperm were incubated for 8 h with the cell-permeable ceramide N:-hexanoylsphingosine (25 microM) or with solvent. Ceramide increased the incidence of progesterone-responsive sperm and, at later times, spontaneously reacted sperm. N:-Hexanoylsphinganine, an inactive control ceramide, had no effect. These results suggest that sphingomyelin in the sperm influences the rate of capacitation by slowing the loss of sterols, and that exogenous sphingomyelinase accelerates capacitation by speeding the loss of sterols and by generating ceramide.

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Section: Discussionmentioning

confidence: 99%

Sphingomyelin Modulates Capacitation of Human Sperm In Vitro1

Cross

2000

Biology of Reproduction

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“…A messenger role for ceramide in cells activated by tumour necrosis factor (TNF)-α [17,18], transforming growth factor-β [19], and 1α,25-dihydroxyvitamin D 3 [19] has been demonstrated. In human spermatozoa, the involvement of a sphingomyelin/ceramide pathway has been suggested as playing a role in the capacitating processes [21], and a neutral sphingomyelinase has been identified in ram spermatozoa [22]. However, the role of ceramide in the mechanism underlying acrosomal exocytosis has not yet been investigated.…”

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confidence: 99%

Ceramide Enhances Acrosomal Exocytosis Triggered by Calcium and the Calcium Ionophore A23187 in Boar Spermatozoa

Murase

Imaeda

Kondoh

et al. 2004

Journal of Reproduction and Development

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Abstract. Mammalian spermatozoa must undergo acrosomal exocytosis prior to penetration of the oocyte at fertilization. The mechanisms underlying acrosomal exocytosis have not yet been fully elucidated. This study explored the possible involvement of ceramide in exocytosis of the boar sperm acrosome. Ejaculated boar spermatozoa, stored with the Beltsville TS extender at 17C for up to 3 days, were washed and preincubated for 10 min with C2-ceramide, an analogue of endogenous ceramide, C2-dihydroceramide (C2-DH-ceramide), a negative control to C2-ceramide, or with (1S,2R)-D-erythro-2-(N-myristoylamino)-1-phenyl-1-propanol (D-erythro-MAPP), an inhibitor of alkaline ceramidase, followed by incubation and stimulation with 3 mM Ca 2+ and 0.3 µM A23187 (Ca 2+ /A23187) at 37C in air in a water bath. Spermatozoa fixed at specific intervals were examined, and the % of acrosomal exocytosis was monitored. Stimulation of spermatozoa with Ca 2+ /A23187 resulted in a timedependent increase. There were no obvious changes at 5 min, but this was followed by a rapid increase at 10 min, reaching nearly a maximum level after 15 min or more of incubation. Preincubation with C2-ceramide or D-erythro-MAPP enhanced acrosomal exocytosis triggered by Ca 2+ /A23187 in a dose-dependent manner, whereas C2-DH-ceramide was without effect. These results suggest the possibility that ceramide may be involved in the mechanisms underlying acrosomal exocytosis.

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“…For example, ram sperm contain a Mg 2ϩ -depen-dent neutral sphingomyelinase in the plasma membrane and an acidic sphingomyelinase in the sperm homogenate. 17,18 Because no acidic activity was found in the membrane fraction of sperm, it was presumed that ASM was a soluble component of the acrosome.…”

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Reproductive Pathology and Sperm Physiology in Acid Sphingomyelinase-Deficient Mice

Butler

Gordon

et al. 2002

The American Journal of Pathology

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Types A and B Niemann-Pick disease (NPD) are lysosomal storage disorders resulting from the deficient activity of acid sphingomyelinase (ASM). In this manuscript we report the pathobiology of male gonadal tissue and sperm in a knockout mouse model of NPD and demonstrate the importance of ASM for normal sperm maturation and function. Characteristic lipid-filled vacuoles were evident in light micrographs of testis' seminiferous tubules and epithelial cells lining the epididymis of ؊/؊ mice. Electron micrographs extended these findings and revealed storage vesicles within Sertoli cells of the seminiferous tubules. Mature spermatozoa from ؊/؊ mice showed marked ASM deficiency and elevated levels of sphingomyelin and cholesterol. Flow cytometric analysis revealed that affected spermatozoa had disrupted plasma and acrosome membranes, and mitochondrial membrane depolarization. They also did not undergo proper capacitation. Morphological abnormalities such as kinks and bends at the midpieceprinciple piece junction were evident in spermatozoa from affected mice, with consequent deficits in motility. Notably, the mutant sperm regained normal morphology on incubation in mild detergent, demonstrating that the bending defects were a direct consequence of membrane lipid accumulation. A mechanism for these abnormalities is proposed that suggests lipid accumulation in the gonads results in regulatory volume decrease defects within the developing sperm, and that regulatory volume decrease defects, in turn, lead to the observed abnormalities in sperm morphology and function. These results provide in vivo evidence that ASM activity plays a critical role in sperm maturation and function, and a basis for similar studies in sexually mature, male NPD patients. 1 Type A NPD is a severe, neurodegenerative form of the disorder that generally leads to death by ϳ3 years of age. In contrast, patients with type B NPD have little or no neurological involvement and may survive into adolescence or adulthood. ASM belongs to a family of sphingomyelinases that catabolize sphingomyelin (SPM) to ceramide and phosphorylcholine. 2,3 It is presumed that the pathophysiology in NPD is primarily because of the accumulation of SPM and other metabolically related lipids (eg, cholesterol) within the cells and tissues of affected patients, although signaling through the ceramide pathway may also be disrupted.

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A neutral sphingomyelinase in spermatozoal plasma membranes

Cited by 22 publications

References 2 publications

Sphingomyelin Modulates Capacitation of Human Sperm In Vitro1

Sphingomyelin Modulates Capacitation of Human Sperm In Vitro1

Ceramide Enhances Acrosomal Exocytosis Triggered by Calcium and the Calcium Ionophore A23187 in Boar Spermatozoa

Reproductive Pathology and Sperm Physiology in Acid Sphingomyelinase-Deficient Mice

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