Ovipository

[ThePiggy]

Is it only females that show this white egg spot?

 

[modaz]

NOPE

 

[Netty]

Not at all. Lots of juvenile males have this too which is another thing that makes it difficult to sex them accurately.

 

[ThePiggy]

Darn... Of course nature couldn't make it easy for us, eh?

 

[modaz]

Not at all. Lots of juvenile males have this too which is another thing that makes it difficult to sex them accurately.

oh nice sutble way of saying that your useless at sexing bettas ohhh i like your new banner

 

[Netty]

Darn... Of course nature couldn't make it easy for us, eh?

It certainly doesn't.......but what fun we have along the way

Not at all. Lots of juvenile males have this too which is another thing that makes it difficult to sex them accurately.

oh nice sutble way of saying that your useless at sexing bettas ohhh i like your new banner

makes 2 of us then lol.

Cheers......website should go live tomorrow night, fingers crossed. Watch this space

 

[ThePiggy]

Yeah, fun like trying to start a sorority and finding all your females cowering because of the accidental young male was introduced... tons-o-fun

 

[modaz]

Yeah, fun like trying to start a sorority and finding all your females cowering because of the accidental young male was introduced... tons-o-fun

Oh those days, thats why i house all females seperately now, i learnt the hard way.

Netty.... dont say things like that about Plakat

 

[Netty]

What.....surely not 3 of us

Separating girls is definately the way foward.....just means lots more tanks....yay!!!!!

 

[modaz]

What.....surely not 3 of us

Separating girls is definately the way foward.....just means lots more tanks....yay!!!!!

 

[Syphoniera]

Hi, guys, it's me, again pointing out that it's not nature which has caused fish to develop both sets of sexual equipment, or to feminize males to the point where they produce viable eggs, at increasing rates over the past few decades.
It's industrially produced endocrine disrupting chemicals which can attach to genetic material and mimic hormones, wreaking havoc with cellular signaling in many - and any - respects
This is important, because the situation is worsening.
And unless people become aware, it will continue to do so.
Not only fish are affected, although it's often more noticeable in these.
And there are serious concerns that entire populations of certain fish in various waterways may die out shortly, specifically due to this.
These are not problems isolated to North America and Britain, although most studies/papers/articles I've seen so far appear to be predominately centred in these areas.
This is a world-wide, life-on-Earth-threatening disaster in slow-motion being missed even by those interested in breeding fish - which now all too often develop both sets of sexual equipment or change sex, something most evident in such fish as Bettas, which are individually bred under close supervision, as well as the males being necessarily kept apart from their own species.
And we're accepting this as normal?

An URL to a previous posting on the subject with some info.

http/www.fishforums.net/index.php?showtopic=258980


Such bizarre oddities as feminized/hermaphroditic and other such genetically/hormonally disrupted animals are not 'natural'.
Neither are genetic males which have developed as fully functional females due to artificial chemical-triggered hormonal interference in early development, and males which are identifiable but sterile, and in any case unable to continue their race.
Men - we really can't live without them.
And the same holds true for fish and other animals.

Since this would appear likely to be a dead thread, as far as further comment on the subject is concerned, the following, therefore included, may provide some form of general overview.

http/www.skinner.wsu.edu/Endoreprint.pdf

Epigenetic Transgenerational Actions of Endocrine Disruptors
Matthew D. Anway and Michael K. Skinner
Center for Reproductive Biology, School of Molecular Biosciences, Washington State University, Pullman, Washington 99164

Endocrine disruptors have recently been shown to promote an epigenetic transgenerational phenotype involving a number of disease states (e.g. male infertility). The anti-androgenic fungicide vinclozolin was found to act transiently at the time of embryonic sex determination to promote in the F1 generation a spermatogenic cell defect and subfertility in the male. When the animals were allowed to age up to 1 yr, a number of other disease states developed. This phenotype was transferred through the male germ line to all subsequent generations analyzed (F1-F4). The ability of an environmental factor (i.e. endocrine disruptor) to promote an epigenetic
transgenerational phenotype impacts the potential hazards of environmental toxins, mechanisms of disease etiology, and evolutionary biology. The biological importance of the epigenetic actions of environmental agents is reviewed in the context of the primordial germ cell and development of epigenetic transgenerational phenotypes. (Endocrinology 147: S43-S49, 2006)
GENOMIC DNA CONTAINS the core of genetic information of the cell. There is a distinct pattern of gene expression through out mammalian development that is heritable from parents to offspring. Epigenetics is defined as the molecular phenomena that regulate gene expression without alterations to the DNA sequence (1).
The most studied epigenetic modification is DNA methylation of CpG nucleotides that are essential for mammalian development (2-5)
. DNA methylation of CpG sites is used by mammals to regulate transcription of genes, alter chromosomal positioning, influence X-chromosome inactivation, control imprinted genes, and repress parasitic DNAs (1, 5-9). Alterations in the DNA methylation state can lead to multiple disease states including cancers (10, 11), Rett syndrome, and Prader-Willi/Angelman syndrome (11-13), male infertility (14), autism (12), and Angelman and Beckwith-Wiedemann syndromes (13).
Both chemical and environmental toxins have been shown to alter DNA methylation patterns resulting in epigenetic phenotypes (14, 15).

DNA methylation patterns are established at two times during development: the lineage-specific pattern during gastrulation and the germ-line-specific pattern in the gonad after sex determination (16). The lineage-specific pattern establishes the DNA methylation for somatic cell development after fertilization.
This epigenetic reprogramming is based on the genetic material transferred from the egg and sperm.
Alterations in the lineage-specific epigenetic reprogramming results in developmental defects or embryonic lethality (13,
16). The germ-line DNA methylation pattern is established during gonadal development and is sex specific (16 -18).
Epigenetic reprogramming of the germ line is critical for imprinting (19 -22). Unlike the lineage-specific reprogramming, alterations in the germ-line epigenetic reprogramming can alter the heritable epigenetic information, resulting in a transgenerational phenotype (15) (Fig. 1). The embryonic period is the most sensitive for chemical and environmental effects on the epigenetics of the male germ line (15, 21, 22).
Recent investigations of the DNA methylation state of the germ cells have indicated that as primordial germ cells migrate down the genital ridge, a demethylation (i.e. erasure of methylation) starts, and upon colonization in the early gonad, a complete demethylation is achieved (21-23).

This has been primarily observed through the analysis of specific imprinted genes (24). During the period of sex determination in the gonad, the germ cells undergo a remethylation involving a sex-specific determination of the germ cells
(Fig. 2). Although the demethylation may not require the gonad somatic cells (21), the remethylation of the germ line appears to be dependent on association with the somatic cells in the gonads (22, 23)
. Because of this unique property of the germ cells to undergo a demethylation and the period of sex determination in the developing gonad, the ability of an environmental agent such as an endocrine disruptor to influence through an epigenetic process the germ line is postulated. This epigenetic effect on the germ line could reprogram the germ cell through an event such as altered DNA imprinting (25, 26). This epigenetic effect could cause a transgenerational effect on subsequent generations through the germ line. Because the remethylation of the germ line appears dependent upon the gonadal somatic cells, an alteration in somatic cell function by an agent such as an endocrine disruptor could indirectly influence the germ cell remethylation (Fig.
2). Epigenetic alterations that lead to transgenerational transmission of specific genetic traits or molecular events (e.g. imprinting) have recently been identified (6, 7, 27). These observations have led to the conclusion that a reprogramming through altered epigeneticsof the male germ line is possible (15)
. The impact this has on human health and evolutionary biology is significant (6, 27).
First Published Online May 11, 2006
Abbreviation: AR, Androgen receptor.

(My comment - the last I heard, I believe it was the 9th continuous generation of unexposed test subjects which were found to be still exhibiting the effects of the exposed 1st, and to a greater extent in unexposed descendents than in the original exposed ancestors.
Vinclozolin was one of two chemicals to which we are commonly exposed which were tested and found to produce such effects.
The class of endocrine disrupting chemicals is very large and many of these have been specifically tested for and found in representative sampling of human body burdens of industrial chemicals conducted in multiple countries.)



http/www.pan-uk.org/pestnews/actives/vinclozo.htm


PAN International Website


Vinclozolin
Vinclozolin is a fungicide introduced in the late 1970s. There are current concerns about reproductive toxicity, additive toxicity and potential endocrine disruption that have yet to be resolved.
What is vinclozolin?
Vinclozolin is a protectant non-systemic dicarboximide fungicide used mainly on oilseed rape and peas in the UK(1) and on vines, fruit and vegetables worldwide (2). It was first introduced by BASF in Germany in 1976 and is sold under a number of trade names including Ronilan and Flotilla.
In 1998 23.4 tonnes were used on 80,574 ha of oilseed rape in the UK(3), and approximately 64 tonnes in total in the US(4) in 1999 on a wide variety of crops.

Acute toxicity
Vinclozolin is not acutely toxic, and is classified by the World Health Organisation as 'unlikely to present acute hazard in normal use' (5). The acute oral LD50 (the dose required to kill half a population of laboratory animals) is more than 10,000 mg/kg for rats. It is an irritant to skin and may cause sensitization(6)
.

Chronic toxicity
A recent review of vinclozolin by the US Environmental Protection Agency (EPA)(7) has concluded that the chemical and/or its breakdown products are associated with the development of testicular tumours in rats, and the final breakdown product of vinclozolin in the rat is also thought to be carcinogenic.
Tests on dogs have shown effects on the renal and prostate glands.
It is suggested they are the most sensitive species (8).


Reproductive toxicity
Issues over the reproductive toxicity of vinclozolin have driven regulation for over a decade. The UK Advisory Committee on Pesticides (ACP) has kept vinclozolin under review since 1991(9) following reports of the reproductive effects of the chemical on rats, to assess the risk to consumers and operators. The specific concerns were that vinclozolin could feminize rats and could also damage reproductive capacity in rats. Given that the chemical could be used by operators on a regular basis over quite considerable periods of time, and that a short exposure could have serious consequences for a 'susceptible' individual, and a high proportion of women were employed in the horticultural sector, action was needed.
Approvals for use on strawberries, lettuce, tomato and raspberries were all suspended. Regulatory action was taken to reduce exposure to both by requiring tractor-mounted or trailed downward placement by hydraulic sprayer. Protective clothing requirements were also made.
Further data was submitted to the ACP in 1995, when uses in apple orchards were reinstated provided that the operator was protected by having air
filtration fitted in the tractor cab (10).
The European Union (EU) is currently reviewing the toxicity of vinclozolin. (11)
In 1999, its Scientific Committee on Plants was asked to consider if humans and particularly children might be more sensitive than rats to its effects. The Committee said humans were not more sensitive than animals, and that it was unlikely that a single exposure could cause ill effects. It also considered that the mechanism of toxicity was now established. It did however, note that adverse effects on young animals were generally irreversible, whereas effects on adult animals could generally be reversed. It is likely that as a result the UK ACP will now consider restoring the currently suspended approvals.
In the meantime, the US EPA considers vinclozolin to be an endocrine-disrupting chemical interfering with lipid metabolism and/or storage and inducing reduced sperm count, decreased prostate weight and delayed puberty in test animals. (12) A further question emerging from the EPA review is whether vinclozolin shares a common mechanism of toxicity with the fungicides procymidone and possibly iprodione, and what might be the likely impact of additive exposure.
The European Commission(13) has also indicated vinclozolin as a high priority chemical for investigation of endocrine effects, and the UK Department of the Environment, Transport and the Regions (DETR) (14) has echoed these concerns.

Environmental fate
Vinclozolin is only partially broken down by soil microorganisms, with estimated half lives of three days to more than three weeks depending on soil type. Field data indicate it will be strongly sorbed to moist soils and unlikely to leach significantly (15).

Wildlife
There have been concerns about the possible impacts of vinclozolin on birds. The question was put to the EU's Scientific Committee on Plants and received the
answer that under the conditions of use of vinclozolin in orchards, vineyards and fields there would be no unacceptable risk to wild mammals.

While short term effects on birds and wild mammals would not be expected, possible long term effects on birds could not be excluded (16).
Vinclozolin is said to present a minimal hazard to bees when used as directed, but users are advised to 'consider informing local bee-keepers if intending to spray crops in flower' (17).
It is labeled in the UK as harmful to fish and aquatic life. The US review notes chronic risk to aquatic organisms has not been assessed due to lack of data.

Food residues
In the UK instances of illegal use cause concern. Although there have been no approvals for use on winter lettuce for some years, an enforcement survey (18) found three cases of illegal use in 1997-98, resulting in prosecutions.
One example of illegal use was found on tomatoes in 1998, and strawberries in 1999.
A survey in EU member states and Norway(19) reported on the most frequently occurring pesticide residues in national residue monitoring - vinclozolin was the seventh most frequently reported residue.

Conclusions
Regulators are concerned about potential adverse reproductive impacts of vinclozolin. The EU now appears satisfied but the US EPA remains committed to phasing out most uses of the chemical. The potential impacts of endocrine disruption have to be weighed, and US regulators are also concerned with additive impacts, as vinclozolin may share a common mechanism of toxicity with other fungicides, procymidone and iprodione. (PB)

http/www.nrdc.org/health/effects/qendoc.asp#disruptor


. What is the endocrine system?

The endocrine system is a complex network of glands and hormones that regulates many of the body's functions, including growth, development and maturation,
as well as the way various organs operate. The endocrine glands -- including the pituitary, thyroid, adrenal, thymus, pancreas, ovaries, and testes -- release carefully-measured amounts of hormones into the bloodstream that act as natural chemical messengers, traveling to different parts of the body in order to control and adjust many life functions.


2. What is an endocrine disruptor?

An endocrine disruptor is a synthetic chemical that when absorbed into the body either mimics or blocks hormones and disrupts the body's normal functions. This disruption can happen through altering normal hormone levels, halting or stimulating the production of hormones, or changing the way hormones travel through the body, thus affecting the functions that these hormones control. Chemicals that are known human endocrine disruptors include diethylstilbesterol (the drug DES), dioxin, PCBs, DDT, and some other pesticides. Many chemicals, particularly pesticides and plasticizers, are suspected endocrine disruptors based on limited animal studies.


3. What are some likely routes of exposure to endocrine disruptors?

Exposure to endocrine disruptors can occur through direct contact with pesticides and other chemicals or through ingestion of contaminated water, food, or air. Chemicals suspected of acting as endocrine disruptors are found in insecticides, herbicides, fumigants and fungicides that are used in agriculture as well as in the home. Industrial workers can be exposed to chemicals such as detergents, resins, and plasticizers with endocrine disrupting properties. Endocrine disruptors enter the air or water as a byproduct of many chemical and manufacturing processes and when plastics and other materials are burned. Further, studies have found that endocrine disruptors can leach out of plastics, including the type of plastic used to make hospital intravenous bags. Many endocrine disruptors are persistent in the environment and accumulate in fat, so the greatest exposures come from eating fatty foods and fish from contaminated water.


4. How do we know that endocrine disruptors are dangerous?

Many plant and animal species are showing signs of ill health due to exposure to endocrine disrupting chemicals. For example, fish in the Great Lakes, which are contaminated with polychlorinated biphenyls (PCBs) and other man-made chemicals, have numerous reproductive problems as well as abnormal swelling of the thyroid glands. Fish-eating birds in the Great Lakes area, such as eagles, terns, and gulls, have shown similar dysfunctions.

Scientists have also pointed to endocrine disruptors as the cause of a declining alligator population in Lake Apopka, Florida. The alligators in this area have diminished reproductive organs that prevent successful reproduction. These problems were connected to a large pesticide spill several years earlier, and the alligators were found to have endocrine disrupting chemicals in their bodies and eggs.


5. Should humans be concerned for their health based on evidence that fish, birds and alligators have been affected?

Yes. All vertebrates (fish, amphibians, reptiles, birds, and mammals, including humans) are fundamentally similar during early embryonic development. Scientists can therefore use the evidence acquired on other species to make predictions about endocrine disrupting effects on humans.


6. Is there direct evidence that humans are susceptible to endocrine disruption?

Yes. In the 1950s and 1960s pregnant women were prescribed diethylstilbestrol (DES), a synthetic estrogen, to prevent miscarriages. Not only did DES fail to prevent miscarriages, but it also caused health problems for many of these women's children. In 1971, doctors began reporting high rates of unusual vaginal cancers in teenage girls. Investigations of the girls' environmental exposures traced the problem to their mothers' use of DES. The girls also suffered birth defects of the uterus and ovaries, and immune system suppression.

7. Are children at greater risk from endocrine disruptor exposure?

Yes. Because endocrine disruptors affect the development of the body's vital organs and hormonal systems, infants, children and developing fetuses are more vulnerable to exposure. And as was the case with DES, parents' exposure to certain chemicals may produce unexpected -- and tragic -- effects in their children, even decades later.


8. These days don't chemicals have to be safe to be allowed on the market?

No. The majority of the more than 2,000 chemicals that come onto the market every year do not go through even the simplest tests to determine toxicity. Even when some tests are carried out, they do not assess whether or not a chemical has endocrine interfering properties.

9. What can I do to reduce my risk of exposure?


Educate yourself about endocrine disruptors, and educate your family and friends.
Buy organic food whenever possible.
Avoid using pesticides in your home or yard, or on your pet -- use baits or traps instead, keeping your home especially clean to prevent ant or roach infestations.
Find out if pesticides are used in your child's school or day care center and campaign for non-toxic alternatives.

Avoid fatty foods such as cheese and meat whenever possible.

If you eat fish from lakes, rivers, or bays, check with your state to see if they are contaminated.
Avoid heating food in plastic containers, or storing fatty foods in plastic containers or plastic wrap.
Do not give young children soft plastic teethers or toys, since these leach potential endocrine disrupting chemicals.
Support efforts to get strong government regulation of and increased research on endocrine disrupting chemicals.
Last revised 11.25.98

My comment - now, of course, the chemicals listed above, such as those in pesticides and plastics, as 'suspected' ,are known, endocrine disruptors, and they're in every facet of our lives.
Wild fish don't use, and therefore can't avoid using, these products.
And our Bettas live in our drinking water...


http/www.ehponline.org/members/2005/8068/8068.html


Assessment of Feminization of Male Fish in English Rivers by the Environment Agency of England and Wales
Melanie Y. Gross-Sorokin, Stephen D. Roast, and Geoffrey C. Brighty

Ecosystems and Human Health, Science Group, Environment Agency, Wallingford, Oxfordshire, United Kingdom

Introduction
The Environment Agency's Assessment of the Widespread Feminization of Fish
Identification of Causative Substances
The Environment Agency's Risk Management Strategy
Abstract
In recent years there has been considerable concern over the ability of substances discharged into the environment to disrupt the normal endocrine function of wildlife. In particular, the apparent widespread feminization of male fish in rivers has received significant attention from regulators in the United Kingdom, the United States, Europe, and Japan. The U.K. and European epidemiological data sets have demonstrated that the occurrence of feminized fish is associated with effluent discharges and that the incidence and severity is positively correlated with the proportion of treated sewage effluent in receiving waters. Although weakly estrogenic substances may contribute to the overall effect, studies have concluded that steroid estrogens are the principal and most potent estrogenic components of domestic sewage. Extensive laboratory data sets confirm that steroid estrogens are capable of eliciting the effects observed in wild fish at concentrations that have been measured in effluents and in the environment. Based on evaluation of the available information, the Environment Agency (England and Wales) has concluded that the weight of evidence for endocrine disruption in fish is sufficient to develop a risk management strategy for estrogenically active effluents that discharge to the aquatic environment. Key words: endocrine disruption, ethinylestradiol, feminization, fish, estradiol, estrone, risk assessment, steroid estrogen. Environ Health Perspect 114(suppl 1) : 147-151 (2006) . doi:10.1289/ehp.8068 available via http/dx.doi.org/ [Online 21 October 2005]


--------------------------------------------------------------------------------

This article is part of the monograph "The Ecological Relevance of Chemically Induced Endocrine Disruption in Wildlife."


If we go on accepting this state of things, your Betta won't be the only 'boy named Sue'.

 

[bronzecat]

Juvenile males have always shown an ovispot to some extent. Its their way of avoiding conflict with mature males, sort of a disguise.

No offence Syphoniera, but I personally dont read your posts, especially the ones that are like a novel. There's not enough hours in the day. Its not just you, but when i see reams and reams of copied text it puts me off.

 

[ThePiggy]

Juvenile males have always shown an ovispot to some extent. Its their way of avoiding conflict with mature males, sort of a disguise.

No offence Syphoniera, but I personally dont read your posts, especially the ones that are like a novel. There's not enough hours in the day. Its not just you, but when i see reams and reams of copied text it puts me off.

Do most of the males grow out of this?

(I couldn't read it either. I saw the post and went cross-eyed )

 

[Netty]

They generally do once they are fully mature. I suppose like alot of animals in nature they have ways to camouflage themselves against being attacked.....even by their own kind.

 

[loraxchick]

although long, there is ALWAYS very interesting material given, Syphoneria...makes a person think...usually very scientific and intriguing. right up my alley!