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LETTER TO EDITOR
Adv Biomed Res 2014,  3:129

Metals and male reproduction: The possible mechanisms


Department of Physiology, Vidyasagar College for Women, University of Calcutta, Kolkata, West Bengal, India

Date of Web Publication28-May-2014

Correspondence Address:
Dr. Pallav Sengupta
Department of Physiology, Vidyasagar College for Women, University of Calcutta, 39, Sankar Ghosh Lane, Kolkata - 700 006, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2277-9175.133253

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How to cite this article:
Sengupta P. Metals and male reproduction: The possible mechanisms. Adv Biomed Res 2014;3:129

How to cite this URL:
Sengupta P. Metals and male reproduction: The possible mechanisms. Adv Biomed Res [serial online] 2014 [cited 2019 Oct 23];3:129. Available from: http://www.advbiores.net/text.asp?2014/3/1/129/133253

Sir,

Men are inevitably exposed to metals due to their ubiquity in nature, wide use in industry and long-term persistence in the environment. The information on the most important occupational and environmental sources of metal exposure has mainly been collected from the toxicological profiles issued by the Agency for Toxic Substances and Disease Registry (ATSDR). [1] Metals may affect the male reproductive system directly, when they target specific reproductive organs, or indirectly, when they act on the neuroendocrine system. These effects can be long lasting and irreversible if Sertoli cells are disrupted during the foetal development. The number of Sertoli cells determines the number of sperm produced in adulthood, because each Sertoli cell can support only a finite number of germ cells that develop into sperm. According to Sharpe et al., [2] Sertoli cells proliferate during the foetal, neonatal and pre-pubertal period, and each of these periods is particularly sensitive to the adverse effects of metals. The disruption of spermatogenesis in men at any stage of cell differentiation can decrease the total sperm count, increase the abnormal sperm count, impair the stability of sperm chromatin or damage sperm DNA. [3] Accumulating in the epididymis, prostate, vesicular seminalis or seminal fluid, metals may impair progressive sperm motility. [3] In addition, metals can cause hormonal imbalance by affecting the neuroendocrine system, disrupting the secretion of androgens from Leydig cells or Inhibin B from Sertoli cells. [4],[5] There is growing evidence that oxidative stress is implicated in the pathogenesis of male infertility. [3],[4] It is known that human spermatozoa are particularly vulnerable to oxidative stress. An excessive generation of reactive oxygen species (ROS) in the spermatozoa results in the peroxidation of polyunsaturated fatty acids within their plasma membrane. [3] Several metals, including iron, copper, nickel, lead, calcium and cadmium, may increase ROS production, decrease glutathione and other antioxidant levels, enhance the lipid peroxidation of the cell membrane, cause apoptosis, and contribute to the oxidative damage of DNA. Damage to the sperm membrane reduces sperm's motility and ability to fuse with the oocyte, whereas damage to the sperm DNA compromises paternal genomic contribution to the embryo and increases the risk of infertility, miscarriage, or serious disease in the offspring. [6],[7],[8],[9],[10],[11],[12] Some malformations of the male reproductive system, such as cryptorchidism, hypospadias, and prostate and testicular cancers may originate from exposure to endocrine disruptors. [3],[4],[5] Cadmium, calcium, mercury, lead, and arsenic are suspected to affect the endocrine system. Evidence is usually limited to animal data or to in vitro studies. [4] The clinical and epidemiological findings are scarce and controversial, and often difficult to interpret because of multiple exposures to different agents and latency of effects.

 
  References Top

1.Agency for Toxic Substances and Disease Registry. Atlanta (ATSDR). Toxicological profi le for arsenic 2007. Available from: Http://www.atsdr.cdc.gov/ToxProfiles/tp2.pdf. [Last accessed on 2012 Dec 20].  Back to cited text no. 1
    
2.Sharpe RM, McKinnell C, Kivlin C, Fisher JS. Proliferation and functional maturation of Sertoli cells, and their relevance to disorders of testis function in adulthood. Reproduction 2003;125:769-84.  Back to cited text no. 2
    
3.Chandra AK, Sengupta P, Goswami H, Sarkar M. Excessive dietary calcium in the disruption of structural and functional status of adult male reproductive system in rat with possible mechanism. Mol Cell Biochem 2012;364:181-91.  Back to cited text no. 3
    
4.Sengupta P. Environmental and occupational exposure of metals and their role in male reproductive functions. Drug Chem Toxicol 2013;36:353-68.  Back to cited text no. 4
[PUBMED]    
5.Chandra AK, Sengupta P, Goswami H, Sarkar M. Effects of dietary magnesium on testicular histology, steroidogenesis, spermatogenesis and oxidative stress markers in adult rats. Indian J Exp Biol 2013;51:37-47.  Back to cited text no. 5
    
6.Sengupta P, Chaudhuri P, Bhattacharya K. Male reproductive health and yoga. Int J Yoga 2013;6:87-95.  Back to cited text no. 6
[PUBMED]  Medknow Journal  
7.Sengupta P, Banerjee R. Environmental toxins: Alarming impacts of pesticides on male fertility. Hum Exp Toxicol. 2013. [Epub ahead of print].  Back to cited text no. 7
    
8.Sengupta P. The Laboratory Rat: Relating its age with humans. Int J Prev Med 2013;4:624-30.  Back to cited text no. 8
[PUBMED]  Medknow Journal  
9.Sengupta P, Sahoo S. A Cross Sectional Study to Evaluate the Fitness Pattern among the Young Fishermen of Coastal Orissa. Indian J Pub Health Res Dev 2013;4:171-5.  Back to cited text no. 9
    
10.Sengupta P. Potential Health Impacts of Hard Water. Int J Prev Med 2013;4:866-75.  Back to cited text no. 10
[PUBMED]  Medknow Journal  
11.Dutta S, Joshi KR, Sengupta P, Bhattacharya K. Unilateral and bilateral cryptorchidism and its effect on the testicular morphology, histology, accessory sex organs and sperm count in Laboratory Mice. J Hum Repro Sci 2013;6:106-10.  Back to cited text no. 11
    
12.Krajewska-Kulak E, Sengupta P. Thyroid function in male infertility. Front Endocrinol 2013;4:1-2.  Back to cited text no. 12
    




 

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