Abstract
Recent studies have shown cytoplasmic droplets to be normal morphological occurrences in human male spermatozoa. When the cytoplasm around the sperm midpiece is present in large amounts, however, pathological effects may transpire. The cytoplasmic droplet then becomes known as excess residual cytoplasm, which can impair overall sperm function and produce higher levels of reactive oxygen species, potentially leading to male infertility. Though the distinction between cytoplasmic droplets and excess residual cytoplasm has been made, some studies fail to recognize the difference and incorrectly label the latter as a cytoplasmic droplet. This review attempts to clarify excess residual cytoplasm’s effect on fertility, examine the enzymes responsible, and suggest tests and possible treatment options for those affected by this defect.
Highlights
Male infertility accounts for about half of all infertility cases and may arise from a variety of factors
One known cause is the retention of excess cytoplasm around the midpiece due to an arrest in spermiogenesis and incomplete cytoplasmic extrusion [1]
This is known as excess residual cytoplasm (ERC)
Summary
Male infertility accounts for about half of all infertility cases and may arise from a variety of factors. Studies have suggested the association of ERC with varicocele presence [42] They each cause an increase in ROS production, and both idiopathic and varicocele-related male infertility have been correlated with impaired cytoplasmic extrusion [43]. H2O2 molecules, if left to accumulate, may undergo homolytic cleavage to form two hydroxyl free radicals (OH · -), highly reactive electrophiles that cause oxidative damage to cells [53] (Figure 2) Due to their high phospholipid content and relatively low cytoplasmic volume, spermatozoa are especially susceptible to this condition [34]. Oxidative stress caused by ERC can impair sperm motility and function, affecting capacitation and fertilization [62] It may render the sperm plasma membrane unable to respond to intracellular calcium signals, impeding spermoocyte fusion [63]. This topic merits further investigation to assess the efficacy of this and other treatments
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