Abstract:Bisphenol A enter in aquatic environments through discharged off effluents,principally from industrial plants, commercial areas and have great influenceon variety of aquatic biota, including fish. Evidence for changes of physiologyin fish as a result of exposure of BPA is worldwide, with some of the mostwidely reported impacts on sexual development and function. In recent years,many researches have been done which shown that BPA has great influence on freshwater fishes which result in behavioral changes of individual level and which leadto population level. This review presents a critical assessment on reportedeffects of bisphenol A on behavior in fish, mainly disturbance in reproduction behavior.However, there are many technical and interpretation challenges to predict therole of BPA in endocrinal disruption and there is great debatable point thathow behaviors under laboratory conditions equate with those occurring in wildpopulations.Introduction:Water is fundamental entity for all livingorganisms to live.
A satisfactory, safe, and good water supply should beavailable for every individual and species. This is a duty of water suppliersto provide good drinking quality of water to all living beings. However,quality of drinking water is the affected by the presence of severalenvironmental pollutants, including endocrine disrupting chemicals (EDCs),pharmaceuticals and personal care products (PPCPs), and other substances (Padhye et al.
, 2014). BisphenolA (BPA), one of the most studied EDCs, is an aromatic compound which used allover the world as the precursor of plastics and chemical additives (Vandenberg et al., 2010). BPA is commonly used inthe production of polycarbonate plastics (very common for transparency, heatresistance, and mechanical properties) and epoxy resins for coating of cans offood and beverages.
In aquatic environment, BPA, Pharmaceuticals, pesticides and other chemicals with endocrine disrupting chemicals enter through disposedwastewater, agricultural run-off, and groundwater discharge, which may accumulate both in sediments and in biota include fresh water fisheries(Hu et al., 2005). Fishes are most vulnerableliving organism when introduce to pollutants like BPA because contaminatedwater is directly in contact with fish organs like gills, skin can readilyabsorbed BPA due to continuous exposure with BPA.
BPA can also enter in fishbody through diet and drinking (gut). (Kwong et al., 2008. In some cases,BPA also found in developing eggs which ultimately has influence on embryo andcan retard the development of embryo (Daley et al., 2009). Exposure ofpollutants like BPA and other EDCs canalso cause variations in behavior of fishes in which includes reductionthe capacity for avoidance from predators, reducing/eliminating the ability to detect chemical alarm substances released by conspecifics, affectingschooling behavior, changing feeding behavior, and may change socialhierarchies within a group (Scott and Sloman, 2004). Many studies havebeen conducted to study the effect of BPA on fish physiology, normally onfeatures which relates to growth, development and reproduction (Hutchinson et al., 2006).
In this paper, I present a review of the existingliterature in order to easily identify the current scope of informationavailable regarding effects of Bisphenol A in endocrine disruption for freshwater fish species. This review critically analyses the information whichdetermine the possible effects of BPA, on behavioral changes in fish, mainly onbehaviors related to sex and reproduction. The goal of this review is to determinethe role of BPA in endocrinal disruption of fishes live in freshwater andestuarine fish, in which short-term (i.e., physiology and behavior) and long-termeffects (trans generational) are explained.PossibleMechanisms of Action of BPA as an Endocrine Disrupting Chemical:The general concept is that the estrogenicactivity of BPA is initiated when BPA is attach to estrogen receptors (ERs) in fisheries.BPA has structural similarity to thyroid hormones (THs) because both have 2benzoic rings.
Due to structural similarity with thyroid hormone, BPA act as aTH antagonist or agonist which result in disturbance of the thyroid system andultimately disturbance of whole body functions (Jung et al., 2007). For collection of data, models of fish metamorphosisare mainly used. By using larval stages of fish, Iwamuro et al., (2006) found that in vivo, spontaneous and TH-inducedmetamorphosis is blocked by BPA, as well as in vitro tail cell culture, tailresorption is induced by throid hormones (THS).
Corticotropin-releasing factor(CRF) -inducible release of thyroid-stimulating hormone (TSH) andthyrotropin-releasing hormone (TRH) -inducible release of both TSH and prolactinfrom the pituitary gland are also inhibited by the compound. In fury, the releaseof TSH and prolactin are not regulated by estradiol. This confirms that ERbinding is not related to the release of the pituitary hormones due to BPA. Intail cell culture, the appearance of genes related to metamorphosis is reducedby BPA, which reinforce the hypothesis that effects of BPA are induced bydirectly binding to thyroid hormone receptors rather than estrogen receptors(ERs)(Zoeller, 2005).BPA as Endocrine disrupting chemicals and their biological effects:Inan organism, BPA acts via mimicking or blocking natural hormone functions. An arrayof hormonal systems including estrogen, androgen, progestagen, corticosteroidand thyroid signaling systems are affected by BPA.
Sex steroid action and sexual development and reproductionare seriously affected by BPA. Almost all aspects of reproduction, includingmediating sexual differentiation, gonadal growth, and reproductive behaviorsare controlled by sex steroid hormone (Goodhead and Tyler, 2009).Examinationalefforts show that at comparatively high concentrations (up to 21 µg l?1)of BPA in streams and rivers cause serious biological effects in fisheries.
Results of experiments show that BPA is responsible to cause feminizing effectsin vivo and to induce zona radiata proteins (ZRPs) synthesis in a diverse rangeof fish species. There are few examples of fisheries which are affected atdifferent concentration of BPA i.e. carp 100 µg l?1; fathead minnow160 µg l?1,cod 50 µg l?1,medaka 1000 µg l?1;rainbow trout 500 µg l?1 Lindholst et al. 2001).. In vivo studieshave shown that many other biological processes are influenced by BPA.
Androgenand estrogen synthesis and metabolism disorders are seriously affected byexposure of BPA. Studies have been conducted in carp and results showed that exposure oflow concentrations of BPA (1–10 µg l?1) results in decrease the ratio of estrogen toandrogen in the plasma, while exposure to high concentrations (1000 µg l?1)increases estrogen to androgen ratio (Mandich et al., 2007). Changeswhich are induces in the ratio between estrogens and androgens have biologicalconsequences which are diverse in nature which may comprise masculinization orfeminization of organisms, and/or alterations in other processes controlled bythese hormones (including growth, bone morphogenesis, insulin signaling, neuraldevelopment, cell division and apoptosis). Different studies provide evidencethat different species are sensitive at different concentration of BPA. Forexample, when Atlantic cod (Gadus morhua)and turbot (Scophthalmus maximus) both are exposed to 59 µg BPA l?1via the water, then cod was more vulnerable than turbot because ZRP was more quicklyinduced in the cod than in turbot which can interfere with fertility (Larsen et al., 2006).
Rate of metabolictransformation of BPA is possible reason for variation in sensitivity ofdifferent species when exposed to BPA. Supporting this argument, removal andmetabolism of BPA occur more rapidly in zebra fish (D. rerio) than in the rainbow trout (Oncorhynchus mykiss)(Lindholst et al.
, 2001).Evidence for endocrinedisruption in wild fish Onfish evidence for endocrine disruption in both undomesticated and wildpopulations is broad. Cases of feminized responses in fish, include production of female proteins in males – vitellogenin (VTG), and amendments in germ cell development –production of oocytes in the testis (Lange et al., 2011) in fish exposed to BPA.In the USA reported androgenic reactions include masculinized secondary sex characters in female mosquitofish (Gambusia holbrooki) exposed to BPA(Parks et al., 2001), and androgenic enhancement of secondary sex characters in male fathead minnows (Pimephales promelas) exposed to BPA(Ankleyet al.
, 2003). Effects of BPA on wildfish populations have not yet been clearly explained, although numerousmodeling analyses have tried to report this issue Effects of BPA (estrogens)in fish:Estrogenicproperties of BPA were first reported in 1936. Wide range of (anti-)estrogenic effects and influences have been investigated in a wide-ranging series of laboratory sudies.Zebrafish (Danio rerio), medaka (Oryzias latipes), fathead minnow, and three-spined stickleback (Gasterosteus aculeatus) aremostly used model species fisheries which are used to investigate the impactsof BPA (Ankley and Johnson, 2004). Reproductive organs are mostly affected byestrogens. Estrogens can skew the sex ratio towards females, reduce or preventspermatogenesis and delay maturation ofthe ovaries at higher concentration of BPA(Weber et al.
, 2003).Endocrinaldisruptor chemicals (BPA) can cause increasing masculinizing effect on males, increasing testis size and speed up spermatogenesis. Ovulation and manufacture ofVTG or yolk in females, skew sex ratio towards males and lessening ovary sizeare adverse effects of BPA in females (Seki et al., 2005). Some of the effects of BPA couldlessen the production of offspring which are documented through controlledlaboratory studies and therefore have a population significance.
Effects on reproductivedevelopment and fertility has been revealed due to exposure of environmentalestrogensWhenendocrine-disrupting chemicals such as BPA are introduce in fisheries habitat,the possible adverse effects of these pollutants are not only passed on totheir offspring, but also onto their offspring’s offspring, and their offspringtoo. Ramji et al., (2015) selected Medaka fish for this study due to theirshorter generations, which made it the perfect candidate for the research studyat hand. Results showed a 30% decrease in the fertilization rate of fish, two generationsafter exposure and 20% reduction afterthree generations. If those trends sustained, the potential for declines inoverall population numbers might be expected in generations.Inthe work of Nash et al. (2004) it was shown that exposure to BPA (5 and 0.
5ng/L) had no chief effects on reproductive production, growth, or fertilizationin the F0 generation of fishes. However, when the interaction was continuedinto the F1, their breeding was intensely affected and the population failedcompletely due to reduced sperm quality /infertility in the males. Surprisingly the sterile males still showedtypical male spawning behavior. These consequenceswere confirmed on a larger scale when a lake in Canada dosed with 4-6 ng/L over a period of 3 years caused in the failure of the fathead minnow population, which then consequently recovered two years after cessation of dosing (Kidd et al., 2007). When addressing population level effects of BPA, however,extrapolating between laboratory conclusions and effects in the wild is generally more difficult. Additionally, wild populations are normally exposed to BPAwith diverse means ofaction, rather than a single chemical exposure, as occurs in most laboratory studies.
Reproductive anddevelopmental toxicity of BPA:· Malereproductive effectsThereis abundant qualitative evidence of BPA to cause toxic effects on reproductiveand developmental toxicity to aquatic organisms. Environmental toxicology ofBisphenol A (BPA) was reviewed by Crain etal. (2007), who conclude that BPA can cause disruption of endocrine systemof a diversity of species at environmentally relevant concentrations of 21 µg/Lor less. Reported male reproductiveeffects include: apotosis of testicularcells in swordtail freshwater fish, inhibition of gonadal growth andspermatogenesis in fathead minnows (Sohoni etal., 2001), reduced sperm density & motility in brown trout, decline oftestosterone and 11-ketotestosterone in turbot (Labadie and Budzinski, 2006),and introduction of an intersex condition known as ?testis–ova? in medaka(Metcalfe et al., 2001). Additionally,when BPA exposed to male medaka at concentration and placed with fertilefemales, then as a result, reduced number of eggs and hatchlings were observed;When BPA concentrations of 0.
3, 1 and 3 µmol/L were introduce in fresh waterfisheries habitat, then there was no significant impacts were observed (Shiodaand Wakabayashi, 2000).. · Femalereproductive effects: Different impacts of exposure of BPA ondifferent species of female fresh water fisheries were reported whichinclude: reduction of gonadal growth andegg production in fathead minnows (Sohoni etal., 2001), reduced hatchability of in flathead minnow larvae, delay in, orcomplete stoppage of ovulation in brown trout (Lahnsteiner et al., 2005), less number of eggs and hatchlings in medaka, introductionof Atlantic salmon eggshell zona radiata protein and increased choriogenin mRNAexpression in medaka (Tyl et al.,2002).
When BPA expose for 3 weeks at concentration of 59 µg/L, it will resultin promotion of estrone level in turbot. Both morphological and histological effects on salmon yolk-sac fry wereobserved at high concentration of BPA. At three concentrations (10, 100 and1000 µg/L) of BPA,variations were observed in behaviour, morphology and histologicalstructure which includes fluid accumulation (oedema) in the yolk sac andhaemorrhages in the front part of the yolk sac and in the head around the gillarches at 1000 µg/L. In medeka, at 200 µg/L of BPA, embryo lesions and deformitieshave been observed.
BPA also have effects on the offsprings which includesembryo lesions and deformities at 200 µg/L, and yolk-sac hemorrhages and edemaat 1000 µg/L (Honkanen et al., 2004). Dominance of Femalefisheries:Comprehensiveinformation on some 25,000 fish from approximately 25 different populations wasgathered from Dutch database on freshwater bream populations. It was assumedthat the normal sex ratio should be equivalent, examination of these populationwere conducted and results showed that 11 of them had considerably more femalesthan males. In most cases, between 60 and 65% of the fish were female, but inone case, more than 70% of the fish were female.
Significant majority of maleswere not observed in any case. (Oehlmann et al,2000).Sexratio data on fish populations can affect by many factors but introduction toenvironmental BPA could be one interpretation of these data. Obviously, causeand effect can never display by this type of investigation, but it does atleast increase the possibility of the influences of endocrine disruption at thepopulation level but the question of toxic impacts of estrogenic emissions on allfish populations is one of the most important that still needs to be answered Overview on the effectof BPA on reproductive behaviors in fish Onfresh water fisheries, Many laboratory studies have been conducted which haveshown effects of BPA on reproductive behavior in individuals, with mainly focuson males to show the impact of BPA. The adverse impacts of BPA on male freshwater fisheries include disruption of nest building in adult male, delayedonset of nest building or reduced care for the nest have all been reported. Insand gobies exposure of adult fish to 4 ng /L was shown Reduction in ability of males to gain and keep a nest and reduced their display of sexual behaviors was observed in sandgobies when exposed at high concentration of BPA (Saaristo et al., 2009). Similarly, reduced care for the spawning site wasobserved in adult male fathead minnows when exposed to higher concentration at20 ng/L of BPA (Salierno and Kane, 2009).
Similarly, diminished courtingresponse towards males and had lower reproductive success in females wasobserved when exposed to BPA(at 9.86 ng/L) than unexposed females.Criticalanalysis: Overall,from available data in fresh water fisheries which have been collected fromexperiments, there is agreement on the fact that BPA is a chemical which causetoxic hazards for the ecosystem. In many cases, BPA cause such toxic effects whenits concentration exceed the optimum range in environment. The impacts of life-longanimal exposure to BPA cannot account in laboratory studies, since fish speciesare continuously exposed of BPA and BPA continuously released in large amountsin habitat of fresh water fisheries.
Thus, an underestimation of the effects ofBPA in laboratory experiments is possible, additionally considering thatwildlife species may be exposed to higher BPA concentrations in matrices(leachates, plants effluents, river etc). Differences in behavior, includingboldness, shoaling, startling response, or anxiety, do occur between differentstrains of laboratory zebrafish and zebrafish of different origins and betweendifferent wild populations. Someof behavioral changes are not always easily measured, nor can then beattributed to specific BPA or even modes of action. BPA.
Not only sexualbehaviors are affected by BPA but non-sexual behaviors are also affected by BPA. When experiments are performed to understandthe effects of single concentration of BPA on behavior in wildfish, then wildfish may experience multiple chemical exposure events at a same time which mayincrease the complexity for interpreting behavior responses.Tostudy the effects of BPA on fish behavior, one of the greatest challenges is translating them to the population level. Much of this depends onthe significance of the behavior trait to successful reproduction. When malefemale interactions is prevented orreduced due to exposure of BPA in the spawning process and this occurs for the whole population, as a result, population becomes extinct, even if the individuals are capable of producingviable gametes. Mostof the information fish has come from laboratory studies, on a very limitednumber of fish species which describe the effects of BPA on sexual behavior infresh water fisheries.
Furthermore, most of these studies have been done on laboratorystrains in which population maintained in captivity for many generations whichdefinitely are not true representatives of wild life fisheries sample. In general,lower tolerance and phenotypic variability have been observed in both individualsand populations with lower genetic diversity. .Ourcurrent understanding of the role of BPA in behavioral changes in reproductionand population maintenance is still very limited and very little work has been conducted which show the link between genetic diversity and responses in behavior when there is exposed of BPA in either laboratory or wild populations. So. Arguably a lot of fundamental research work is requiredto obtain a more detailed understanding of fish sexual behaviors andimplications for alterations in these behaviors before they can be applied intoa risk assessment framework, or into predictive population modeling. Conclusion:Inconclusion, the collective findings in this review indicate that BPA can affectsexual behaviors with reproductive consequences for fresh water fisheries andpotentially fish populations.
The different studies which have been conductedon very limited number of species of fish and results showed changes in behavioral phenotypes of fresh water fisheries are notnecessarily specific to BPA. Future efforts should done to increase anunderstanding of role of BPA as endocrinal disruptor which threaten fresh waterfish population as well as species.Recommendations:Ø Developa full toxicological assessment on BPA to determine an acceptable freshwaterexposure level.Ø Identifywhich fresh water species are most at risk to environmental BPA levels.Ø Performmore studies in the natural environment to evaluate real concentrations andlong-term exposures.Ø Investigatethe relative importance of different exposure pathway to BPA (digestive tractand respiratory surfaces) for wildlife.Ø Evaluatethe bioaccumulation potential of BPA, especially in edible species.