An estrogen-inducible screen was developed in yeast (Saccharomyces cerevisiae) in order to assess whether surfactants and their major degradation products are estrogenic. The DNA sequence of the human estrogen receptor (hER) was integrated into the yeast genome, which also contained expression plasmids carrying estrogen-responsive sequences (ERE) controlling the expression of the reporter gene lac-Z (encoding the enzyme β-galactosidase). Thus, in the presence of estrogens, β-galactosidase is synthesized and secreted into the medium, where it causes a color change from yellow to red. This recombinant strain was used to determine whether representatives of major surfactant classes and some of their principal degradation products possess estrogenic activity. The results were compared to the effects of the main natural estrogen 17β-estradiol. None of the parent surfactants tested possessed estrogenic activity. However, one class of surfactants, the alkylphenol polyethoxylates, degrade to persistent metabolites that were weakly estrogenic. Another group of degradation products, the sulfophenyl carboxylates, which are derived from the biodegradation of linear alkylbenzene sulfonates, do not appear to possess estrogenic activity.

Estrogenic activity of surfactants and some of their degradation products assessed using a recombinant yeast screen

A rapidly increasing number of chemicals, or their degradation products, are being recognized as possessing estrogenic activity, albeit usually weak. We have found that effluent from sewage treatme...

https://bura.brunel.ac.uk/bitstream/2438/795/1/Vitellogenesis.pdf

Vitellogenesis as a biomarker for estrogenic contamination of the aquatic environment.

Male reproductive health has deteriorated in many countries during the last few decades. In the 1990s, declining semen quality has been reported from Belgium, Denmark, France, and Great Britain. The incidence of testicular cancer has increased during the same time incidences of hypospadias and cryptorchidism also appear to be increasing. Similar reproductive problems occur in many wildlife species. There are marked geographic differences in the prevalence of male reproductive disorders. While the reasons for these differences are currently unknown, both clinical and laboratory research suggest that the adverse changes may be inter-related and have a common origin in fetal life or childhood. Exposure of the male fetus to supranormal levels of estrogens, such as diethlylstilbestrol, can result in the above-mentioned reproductive defects. The growing number of reports demonstrating that common environmental contaminants and natural factors possess estrogenic activity presents the working hypothesis that the adverse trends in male reproductive health may be, at least in part, associated with exposure to estrogenic or other hormonally active (e.g., antiandrogenic) environmental chemicals during fetal and childhood development. An extensive research program is needed to understand the extent of the problem, its underlying etiology, and the development of a strategy for prevention and intervention.

Male reproductive health and environmental xenoestrogens

It is becoming evident that an increasing number of widely used industrial and agricultural chemicals are estrogenic. The biodegradation products of a major group of nonionic surfactants, the alkylphenol polyethoxylates, are one such group. Some of these chemicals are widespread aquatic pollutants, and bioconcentrate in aquatic biota. Exposure of male rainbow trout (Oncorhynchus mykiss) to four different alkylphenolic chemicals caused synthesis of vitellogenin, a process normally dependent on endogenous estrogens, and a concomitant inhibition of testicular growth. The magnitude of these estrogenic effects was dependent on the estrogenic potency of the chemical, the stage of reproductive development of the fish, and the concentration of the chemical in the water. These results support the contention that exposure of wildlife to environmentally persistent estrogenic chemicals can result in deleterious reproductive consequences.

Inhibition of testicular growth in rainbow trout (Oncorhynchus mykiss) exposed to estrogenic alkylphenolic chemicals

In recent years, a number of man-made chemicals have been shown to be able to mimic endogenous hormones, and it has been hypothesized that alterations in the normal pattern of reproductive development seen in some populations of wildlife are linked with exposure to these chemicals. Of particular importance are those compounds that mimic estrogens and androgens (and their antagonists), because of their central role in reproductive function. In fact, the evidence showing that such chemicals actually do mimic (or antagonize) the action of hormones in the intact animal is limited. In only a few cases have laboratory studies shown that chemicals that mimic hormones at the molecular level (in vitro) also cause reproductive dysfunction in vivo at environmentally relevant concentrations. In addition, the reported studies on wild populations of animals are limited to a very few animal species and they have often centered on localized 'hot-spots' of chemical discharges. Nevertheless, many of these xenobiotics are persistent and accumulate in the environment, and therefore a more widespread phenomenon of endocrine disruption in wildlife is possible. This article reviews the evidence, from both laboratory and field studies, that exposure to steroid hormone mimics may impair reproductive function and critically assesses the weight of evidence for endocrine disruption in wildlife.

Endocrine Disruption in Wildlife: A Critical Review of the Evidence

Bioaccumulation of 4-nonylphenol in marine animals--a re-evaluation.

Biodegradation of 4-nonylphenol in seawater and sediment.

Lethal and sublethal toxicity of 4-nonylphenol to the common mussel (Mytilus edulis L.)

It is well-known that suspended solids in water adsorb hydrophobic pollutants, thereby decreasing the bioavailability of the compounds to aquatic organisms which do not use the particles as food. It is also known that hydrophobic pollutants deposited in sediments usually have a low bioavailability. The relative contribution of water and sediment respectively to bioaccumulation of hydrophobic pollutants has been discussed in many papers based on field data, but the conclusions are uncertain. However, very few studies have been performed under controlled conditions in the laboratory on how the bioaccumulation of such compounds dissolved in the water is changed by adsorption to particles when these particles are used as food by the organism. This has now been investigated using the deposit-feeding bivalve Abra nitida which was exposed to hexachlorobenzene and lindane by means of a new method for dosing of hydrophobic compounds to a continuous flow system in long term tests.

R. Ekelund

Papers

Bioaccumulation of 4-nonylphenol in marine animals--a re-evaluation.

Biodegradation of 4-nonylphenol in seawater and sediment.

Lethal and sublethal toxicity of 4-nonylphenol to the common mussel (Mytilus edulis L.)

Influence of suspended solids on bioavailability of hexachlorobenzene and lindane to the deposit-feeding marine bivalve, Abra nitida (Müller).