http://aerg.canberra.edu.au/library/sex_general/2002_Devlin_Nagahama_sex_determination_in_fish_review.pdf

Sex determination and sex differentiation in fish: an overview of genetic, physiological, and environmental influences

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

Prostate cancer is the second most frequent cancer diagnosis made in men and the fifth leading cause of death worldwide. Prostate cancer may be asymptomatic at the early stage and often has an indolent course that may require only active surveillance. Based on GLOBOCAN 2018 estimates, 1,276,106 new cases of prostate cancer were reported worldwide in 2018, with higher prevalence in the developed countries. Differences in the incidence rates worldwide reflect differences in the use of diagnostic testing. Prostate cancer incidence and mortality rates are strongly related to the age with the highest incidence being seen in elderly men (> 65 years of age). African-American men have the highest incidence rates and more aggressive type of prostate cancer compared to White men. There is no evidence yet on how to prevent prostate cancer; however, it is possible to lower the risk by limiting high-fat foods, increasing the intake of vegetables and fruits and performing more exercise. Screening is highly recommended at age 45 for men with familial history and African-American men. Up-to-date statistics on prostate cancer occurrence and outcomes along with a better understanding of the etiology and causative risk factors are essential for the primary prevention of this disease.

/pdf/epidemiology-of-prostate-cancer-3h05wpx8p6.pdf

Epidemiology of Prostate Cancer

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

Detergent components in sewage effluent are weakly oestrogenic to fish: An in vitro study using rainbow trout (Oncorhynchus mykiss) hepatocytes

Neonatal exposures to technical methoxychlor alters ovaries in adult mice

Effects of the insecticide chlordecone (Kepone) on female reproduction in birds and mammals were reviewed. In different avian species, chlordecone inhibited or reduced reproduction and decreased egg hatchability and survival of the newborn. In Japanese quail, chronic chlordecone ingestion decreased total egg production and clutch size and increased egg breakage. Eggs produced by treated quail were significantly weaker and thinner. Chlordecone also decreased follicular development, induced ovarian regression, and inhibited ovulation and egg laying. Histological studies showed that when chlordecone was fed to sexually immature quail, the oviducts exhibited accelerated growth, cytodifferentiation, cellular hypertrophy, secretory activity, and maturation. Ultrastructure of the oviduct surface showed increased growth of microvilli and profuse ciliation. Chlordecone also stimulated granular endoplasmic reticulum and Golgi development and induced full secretory activity in the cytoplasm of estrogen‐sensitive qua...

Victor P. Eroschenko

Papers

Neonatal exposures to technical methoxychlor alters ovaries in adult mice

Estrogenic activity of the insecticide chlordecone in the reproductive tract of birds and mammals

Effects of progesterone and estrogen on the histology of the oviduct of the garter snake, Thamnophis elegans

Altered behaviors in male mice, male quail, and salamander larvae following early exposures to the estrogenic pesticide methoxychlor.

Estradiol or methoxychlor stimulates estrogen receptor (ER) expression in uteri