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Bisphenol A BPA is widely used in manufacturing industries. It is commonly detected in the environment and was reported to exert oestrogenic effects which may be harmful to the reproductive system. The present study was carried out to observe the effects of oral administration of BPA on the development of the reproductive organs and plasma sex hormone levels in prepubertal male Sprague-Dawley SD rats.

The control animals received the vehicle for BPA Tween 80 in distilled water. Following 6 weeks of BPA exposure, the rats exhibited less evidence of spermatogenesis. There was seminiferous epithelial damage which included disruption of intercellular junctions and sloughing of germ cells into the seminiferous tubular lumen.

Furthermore, the lumina of the seminiferous tubules and the epididymis of these animals were filled with immature germ cells and cellular debris. This damage may lead to the significant reduction in the seminiferous tubular diameter in BPA-treated animals. There was no significant difference between the body weight gain, the absolute as well as relative testis weight or epididymal weight of BPA-treated animals when compared to the control animals. The findings provided further evidence of the detrimental effects of BPA on the male reproductive system.

Various endocrine disrupting chemicals EDCs are commonly used in daily life. These chemicals are also present in the environment and prove to be harmful to human and animals. The environmental contaminants affect normal functions of the endocrine and reproductive systems either by mimicking or inhibiting endogenous hormone actions, or modulating the synthesis of hormones Sonnenschein and Soto, [ 26 ].

The developmental stage embryonic, fetal and juvenile is sensitive to EDC Kavlock et al. Exposure of the fetus to some oestrogenic compounds alters the growth and development of the reproductive organs that may lead to infertility or cancer Naciff et al. An oestrogenic EDC can cause alteration in the hypothalamus-pituitary-testicular axis leading to dysfunctional reproductive system later in adulthood Ramos et al.

Human exposure to BPA may originate from various sources and routes, including leaching from plastic lining of food cans, polycarbonate baby bottles, white dental fillings and sealants Brotons et al. BPA exposure does not always occur only in the adult period, rather it even occurs in the foetal and neonatal period and the toxicokinematics is different in foetuses and neonates Viberg and Lee, [ 31 ].

A European study described that migration of bisphenol A diglycidylether BADGE occurs in all species with relation to storage time-dependent manner, content of fat and the migration is not affected by sterilization conditions. Studies reported that these products leach BPA, which causes contamination of the environment thereby resulting human exposure and uptake in day-to-day life Viberg and Lee, [ 31 ]. Interestingly, BPA has also been detected in the body fluids and tissues such as saliva, breast milk, placenta, amniotic fluid, blood and serum Vandenberg et al.

BPA has also been documented as a potential endocrine disruptor and testicular toxicant D'Cruz et al. This clearly indicates that human exposure to this endocrine disruptor is inevitable and warrants an assessment for the risks involved. Keeping the above facts in mind, the present study was undertaken to observe the effect of BPA on the development and hormonal status in experimental animals.

An earlier study showed that mitochondrial enzymes in the testis such as succinate dehydrogenase, malate dehydrogenase, isocitrate dehydrogenase, monoamine oxidase and NAD dehydrogenase decreased in mice exposed to BPA Anjum et al. BPA has been described to induce the conversion of xanthine dehydrogenase into xanthine oxidase in the rat liver thereby increasing the reactive oxygen species ROS Sakuma et al. The risk assessment studies for BPA invariably used animal models such as rats and mice.

Previous studies on BPA were mostly performed on prenatal animals. The rate at which BPA is cleared from the body system was reported to be dependent on the age and gender of the animal Matsumoto et al. The free level of BPA remains much longer in the body system of neonatal rats compared to the adults Matsumoto et al.

Their capacity to metabolize BPA was found to be increased in relation to the age of the animals Domoradzki et al. The effects of BPA on pubertal development of the reproductive system still remain unclear. Many of the past studies focused on the reproductive system but there is paucity of literature on the histological studies with concomitant observation on the hormonal status.

Majority of the population in the developing countries may not be aware of the harmful effects of BPA on the human body. Therefore, the present study was aimed to observe the effects of exogenous BPA on pubertal development of pre-pubertal male Sprague-Dawley SD rats. They were fed with rodent feed Gold Coin Feedmills Pte.

Animals were allowed to acclimatise for one week prior to treatment on PND Body weights of the rats were recorded weekly. At the end of the experimental period, animals were anesthetized under diethyl ether followed by an intraperitoneal injection of chloral hydrate BDH, England on PND 70 and sacrificed. Selected reproductive organs were harvested and weighed.

The weight of these organs was recorded and then standardised against the body weight to obtain relative organ weights. Testes were examined and the seminiferous tubule diameter was measured using an image analyzer Wetzlar, Germany. No difference in the absolute as well as relative weights of the testis, epididymis, seminal vesicle and prostate between the control and the BPA-treated groups was observed. The testes of the BPA-treated animals exhibited morphological changes compared to the control testes.

While normal patterns of spermatogenesis were observed in the control animals Figure 3A Fig. This was supported by the presence of immature germ cells in the lumen of the seminiferous tubules even with the lowest dose of BPA Figure 3B Fig. Majority of animals in the treated groups did not have mature sperms in their seminiferous tubular lumen.

Furthermore, the epididymal tubules of the control animals contained maturing spermatozoa Figure 4A Fig. Male infertility is one of the major reproductive disorders that warrant public concern. This disorder has been associated with oestrogenic compounds such as BPA Toppari et al.

This happens because of incomplete polymerization during manufacturing or depolymerization caused by increase of temperature induced intentionally sterilisation purpose or unintentionally storage in warehouse Brotons et al.

The results of the present study indicate that exposure of prepubertal male rats to BPA below, at and above NOAEL PND consistently showed some degree of disruption in the morphology and function of the testes.

However, there were no significant changes in the absolute and relative weight of the reproductive organs suggesting that BPA did not alter the general growth of their reproductive organs.

A decrease in the weight of reproductive organs in perinatal studies with chronic exposure to BPA was associated with a reduction in the testicular testosterone level.

This may be due to dependency of these glands on androgen for development and maintenance Akingbemi et al. Despite the significant decrease in the plasma testosterone level observed in the BPA-treated animals, the present study did not show any difference in the weight of the reproductive organs of the experimental animals compared to the control animals. Earlier research results showed that prenatal exposure to BPA and arochlor increased the size of the prostate and decreased the epididymal weight Welshons et al.

There are reports of altered differentiation pattern of periductal stromal cells of the ventral prostate following prenatal exposure to BPA Ramos et al. In the present study, it was noted that spermatogenesis was disrupted in all the BPA-treated SD rats. The seminiferous tubules were devoid of spermatozoa even in animals treated with the lowest dose. Furthermore, the seminiferous epithelium appeared to be disintegrating with loosening of the intercellular bridges between germ cells.

Immature germ cells and degenerating germ cells were observed in the tubular lumen. The smaller seminiferous tubule diameter may be attributed to the thinning seminiferous germinal epithelium with the highest dose of BPA. The process of spermatogenesis begins with differentiation of spermatogonia which requires testosterone action.

It is postulated that the low testosterone level may have caused failure of spermatogenesis and disruption of the seminiferous epithelium. The low plasma testosterone level in BPA-treated animals was probably due to interference of proliferative activity and development of Leydig cells in rat Nanjappa et al. This may explain the lack of spermatozoa and the presence of cellular debris in the lumen of the epididymis of BPA-treated rats. In addition, BPA at lower doses has been reported to induce complete degeneration of epididymal epithelium with reduction in the number of spermatozoa of male Wistar rats.

This observation was postulated to be due to either a decrease in serum testosterone or dihydrotestosterone DHT or even as a result of reduction in 5a-reductase, an enzyme required to convert testosterone to DHT Chitra et al.

They concluded that testosterone production was reduced possibly due to a direct action of BPA on Leydig cells. A recent study reported that BPA caused a reduction in the number of Leydig cells as well as the testosterone levels following 6 weeks of subcutaneous administration Nakamura et al. The research findings indicated that BPA exposure is not only affecting the development and function of the reproductive organs at puberty but also throughout adulthood Akingbemi et al.

The results of the present study provide further evidence to the adverse effects of BPA on the pubertal development of the reproductive system of male SD rats even at a level lower than NOAEL. The most significant effects of BPA were: In line with the recommendation by the World Health Organization, The Malaysian Health Ministry has imposed a ban on the use of polycarbonate infant bottles containing this xenoestrogen beginning early Campaigns for the awareness of BPA containing products such as canned food, plastic food containers and dental sealant and the possible detrimental effects may be increased.

National Center for Biotechnology Information , U. Author information Article notes Copyright and License information Disclaimer. Received Apr 8; Accepted Jan This is an Open Access article distributed under the following Assignment of Rights http: You are free to copy, distribute and transmit the work, provided the original author and source are credited.

This article has been cited by other articles in PMC. Introduction Various endocrine disrupting chemicals EDCs are commonly used in daily life. Hormone analysis At the end of the experimental period, animals were anesthetized under diethyl ether followed by an intraperitoneal injection of chloral hydrate BDH, England on PND 70 and sacrificed.

Morphological analysis Selected reproductive organs were harvested and weighed. Open in a separate window. Mean body weight of rats, mean seminiferous tubule diameters, and mean absolute and relative organ weights of control and BPA-treated rats. Morphological changes The testes of the BPA-treated animals exhibited morphological changes compared to the control testes. Discussion Male infertility is one of the major reproductive disorders that warrant public concern.

Conclusion The results of the present study provide further evidence to the adverse effects of BPA on the pubertal development of the reproductive system of male SD rats even at a level lower than NOAEL. Conflict of interest The authors declare that there are no conflicts of interest. Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol a is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells.

Melatonin ameliorates bisphenol A-induced biochemical toxicity in testicular mitochondria of mouse. Determination of bisphenol-A in reusable polycarbonate food-contact plastics and migration to food-simulating liquids. J Agric Food Chem. Xenoestrogens released from lacquer coatings in food cans. Effect of bisphenol A and co-administration of bisphenol A and vitamin C on epididymis of adult rats: Dental composite fillings and bisphenol A among children: Bisphenol A impairs insulin signaling and glucose homeostasis and decreases steroidogenesis in rat testis:

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