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    Spermatogenesis

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    KRISTOFER BALAIS
    The blood-testis barrier (BTB) is formed by tight junctions between Sertoli cells in the seminiferous tubules of the testes. The BTB divides the tubule into basal and adluminal compartments. It creates a unique microenvironment for germ cell development, protects germ cells from toxic agents, and prevents autoimmunity. A breach of the BTB can impair spermatogenesis by altering the microenvironment, exposing germ cells to toxins, and inducing autoimmunity, potentially causing infertility. Therefore, the BTB plays a crucial role in male reproductive health.

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    Spermatogenesis

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    KRISTOFER BALAIS
    103 views2 pages
    The blood-testis barrier (BTB) is formed by tight junctions between Sertoli cells in the seminiferous tubules of the testes. The BTB divides the tubule into basal and adluminal compartments. It creates a unique microenvironment for germ cell development, protects germ cells from toxic agents, and prevents autoimmunity. A breach of the BTB can impair spermatogenesis by altering the microenvironment, exposing germ cells to toxins, and inducing autoimmunity, potentially causing infertility. Therefore, the BTB plays a crucial role in male reproductive health.

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    What is Blood testis barrier

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    The blood-testis barrier (BTB) is formed by tight junctions between Sertoli cells in the seminiferous tubules of the testes. The BTB divides the tubule into basal and adluminal compartments. It creates a unique microenvironment for germ cell development, protects germ cells from toxic agents, and prevents autoimmunity. A breach of the BTB can impair spermatogenesis by altering the microenvironment, exposing germ cells to toxins, and inducing autoimmunity, potentially causing infertility. Therefore, the BTB plays a crucial role in male reproductive health.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    103 views2 pages

    Spermatogenesis

    Uploaded by

    KRISTOFER BALAIS
    The blood-testis barrier (BTB) is formed by tight junctions between Sertoli cells in the seminiferous tubules of the testes. The BTB divides the tubule into basal and adluminal compartments. It creates a unique microenvironment for germ cell development, protects germ cells from toxic agents, and prevents autoimmunity. A breach of the BTB can impair spermatogenesis by altering the microenvironment, exposing germ cells to toxins, and inducing autoimmunity, potentially causing infertility. Therefore, the BTB plays a crucial role in male reproductive health.

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    DEPARTMENT OF BIOLOGICAL

    SCIENCES
    Visca, Baybay City, Leyte PHILIPPINES
    Telefax: +63 53 563-7536; Local 565-0600 loc. 1019
    Email: [email protected]
    Website: www.vsu.edu.ph

    Biol127 Development Biology


    Kristofer E. Balais
    BS Biology (Zoology) – 3

    Assignment:
    Assignment on Spermatogenesis

    The blood-testis barrier (BTB) is a physical barrier between the blood vessels and the
    seminiferous tubules of the testes. The BTB is formed by tight junctions, adherens junctions
    and gap junctions between adjacent Sertoli cells, which are supporting cells of the
    seminiferous tubules. The BTB divides the seminiferous tubule into a basal compartment
    (outer side of the tubule, in contact with blood and lymph) and an adluminal compartment
    (inner side of the tubule, isolated from blood and lymph).

    The BTB has several important functions for spermatogenesis, which is the process of sperm
    production in the testes. One of its functions is to create a unique microenvironment for the
    development and maturation of meiotic and postmeiotic germ cells (spermatocytes,
    spermatids and sperm) in the adluminal compartment by regulating the chemical
    composition of the luminal fluid. Another function is to protect the germ cells from blood-
    borne toxic agents, such as drugs, hormones, pathogens and antibodies, which can harm
    or destroy them. A third function is to prevent antigenic products of germ cell differentiation
    from entering the circulation and triggering an autoimmune response, since the immune
    system has not been exposed to these products during immune tolerance establishment.
    A fourth function may be to help establish an osmotic gradient that facilitates the
    movement of fluid into the tubular lumen, which is essential for sperm transport and
    ejaculation.

    If the BTB is breached, it can have detrimental consequences for spermatogenesis and
    male fertility. The breach can be caused by trauma, surgery, infection, inflammation or
    genetic defects affecting the junctional proteins. A breach of the BTB can result in alteration
    of the adluminal microenvironment, which can impair the development and function of
    germ cells. It can also result in exposure of germ cells to blood-borne harmful agents, which
    can damage or kill them. Moreover, it can result in induction of an autoimmune response
    against germ cells or their antigens, which can cause orchitis (testicular inflammation),
    DEPARTMENT OF BIOLOGICAL
    SCIENCES
    Visca, Baybay City, Leyte PHILIPPINES
    Telefax: +63 53 563-7536; Local 565-0600 loc. 1019
    Email: [email protected]
    Website: www.vsu.edu.ph

    reduced sperm quality or quantity, or infertility. Therefore, the BTB is a crucial structure for
    maintaining spermatogenesis and male reproductive health.

    References:

    Cheng, C. Y., & Mruk, D. D. (2015). The mammalian blood-testis barrier: its biology and
    regulation. Endocrine reviews, 36(5), 564–591. https://doi.org/10.1210/er.2014-1101

    Jiang, X. H., Bukhari, I., Zheng, W., Yin, S., Wang, Z., Cooke, H. J., & Shi, Q. H. (2014). Blood-
    testis barrier and spermatogenesis: lessons from genetically-modified mice. Asian
    journal of andrology, 16(4), 572–580. https://doi.org/10.4103/1008-682X.125401

    Pelletier, R. M., Byers, S. W., & Wong, V. (2015). The Mammalian Blood-Testis Barrier: Its Biology
    and Regulation. Journal of cellular physiology, 230(10), 2319–2334. https://doi.org/
    10.1210/er.2014-1101

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