Role of acrosomal abnormalities in male infertility

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Abstract

Acrosomal abnormalities are an independent and significant factor in male infertility. One of the key components determining male fertility is the acrosome, a specialized sperm organelle responsible for the acrosome reaction, which enables penetration through the oocyte’s surrounding layers. Acrosome formation occurs during spermiogenesis and involves a complex process of proacrosomal vesicle fusion within the trans-Golgi network. Disruptions in this process may result from genetic defects, particularly mutations in the PICK1, SPATA16, and DPY19L2 genes, leading to acrosomal abnormalities such as globozoospermia, acrosomal hypoplasia, and membrane anomalies. This review summarizes the main mechanisms underlying acrosomal abnormalities. It highlights the association between acrosomal abnormalities and other forms of spermatogenic impairment, such as asthenozoospermia, teratozoospermia, and sperm DNA fragmentation, which significantly reduce the likelihood of conception, even when assisted reproductive technologies are employed. Modern diagnostic methods are described, including electron microscopy, the hyaluronan binding assay (HBA test) for assessing the ratio of mature to immature spermatozoa, and acrosome reaction tests for more accurate detection of subclinical abnormalities. Therapeutic options for these abnormalities were analyzed, including antioxidant and hormone therapy, as well as assisted reproductive technologies such as intracytoplasmic sperm injection, morphologically selected sperm injection, and oocyte activation with ionophores in cases of low fertilization efficiency.

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About the authors

Sergey Yu. Borovets

Academician I.P. Pavlov First Saint Petersburg State Medical University

Email: sborovets@mail.ru
ORCID iD: 0000-0003-2162-6291
SPIN-code: 2482-0230

MD, Dr. Sci. (Medicine), Professor

Russian Federation, Saint Petersburg

Maria K. Frantsishevskaya

Academician I.P. Pavlov First Saint Petersburg State Medical University

Email: potapova_maria_92@mail.ru
ORCID iD: 0000-0002-0288-9777
SPIN-code: 5235-3154

MD, Cand. Sci. (Medicine)

Russian Federation, Saint Petersburg

Svetoslav I. Tereshchenko

City Polyclinic No. 77 of the Nevsky District

Author for correspondence.
Email: teresh555@yandex.ru
Russian Federation, Saint Petersburg

Salman Kh. Al-Shukri

Academician I.P. Pavlov First Saint Petersburg State Medical University

Email: alshukri@mail.ru
ORCID iD: 0000-0002-4857-0542
SPIN-code: 2041-8837

MD, Dr. Sci. (Medicine), Professor

Russian Federation, Saint Petersburg

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2. Fig. 1. Variants of acrosome redundancy: a — acrosome dysplasia, its redundancy, folding, ×14,000; b — acrosome redundancy, its distant position with expansion of the post-acrosomal space (shown by arrows), ×14,000. © Pichugova S.V., 2022. Source: borrowed from [26]. Distributed under the terms of the CC BY 4.0 licence.

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3. Fig. 2. Variants of pathological changes in the acrosome: a, b — non-compact acrosome content; c, d — acrosome degradation (shown by arrows), ×14,000. © Pichugova S.V., 2022. Source: borrowed from [26]. Distributed under the terms of the CC BY 4.0 licence.

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4. Fig. 3. Spermatozoa with normal head shape and abnormal acrosome morphology (1): a — spermatozoon with a reacted acrosome (arrow) and preserved postacrosomal segment (2); b — spermatozoon with enlarged subacrosomal space and absence of the postacrosomal segment (arrow); c — acrosome hypoplasia, abnormally shaped acrosome with unevenly distributed acrosomal matrix substance; d — binuclear spermatozoon with T-shaped acrosome. © Bragina E.E., Bocharova E.N., 2014. Source: borrowed from [27]. Distributed under the terms of the CC BY 4.0 licence.

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