Will we be taught ethics by our clones? The mutations of the living, from endocrine disruptors to genetics

Vandelac, Louise; Bacon, Marie-Hélène

doi:10.1053/beog.1999.0050

Cited by 9 publications

(3 citation statements)

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“…In spite of this high incidence the causes are not well known; unknown etiology, variable pathology, intricate relationship to endocrine factors and anaplastic progression contribute to the complexity of this disease. Further information about the possible harmful consequences of exposure to xenobiotic compounds and the involvement of these compounds in prostate cancer etiology are needed [81].…”

Section: Eds and Cancermentioning

confidence: 99%

Effects of Endocrine Disruptors on Developmental and Reproductive Functions

Brevini¹,

Zanetto²,

Cillo³

2005

curr drug targets immune endocr metabol disord

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Endocrine disruptors (EDs) are exogenous environmental molecules that may affect the synthesis, secretion, transport, metabolism, binding, action, and catabolism of natural hormones in the body. EDs may thus interact with the endocrine system of animals and humans and can exert this effect even when present in minute amounts. EDs have adverse impacts on a number of developmental functions in wildlife and humans. Critical periods of urogenital tract and nervous system development in-utero and during early post-natal life are especially sensitive to hormonal disruption. Furthermore a wide range of hormone-dependent organs (pituitary gland, hypothalamus, reproductive tract) are targets of EDs disrupting effects in adult subjects, possibly resulting in cell transformation and cancer. At present about 60 chemicals have been identified and characterized as EDs and belong to three main groups: (a) synthetic compounds utilized in industry, agriculture and consumer products; (b) synthetic molecules used as pharmaceutical drugs and (c) natural chemicals found in human and animal food (phytoestrogens). In the present review we will give special attention to the family of Polychlorinated biphenyls (also indicated as PCBs) because of their persistence in the environment, ability to concentrate up the food chain, continued detection in environmental matrices, and ability to be stored in the adipose tissue of animals as well as humans. The detrimental effects of these compounds, and of EDs more in general, on health and reproduction will be discussed, presenting experimental data aimed at understanding the molecular mechanisms involved in their action.

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Section: Eds and Cancermentioning

confidence: 99%

Effects of Endocrine Disruptors on Developmental and Reproductive Functions

Brevini¹,

Zanetto²,

Cillo³

2005

curr drug targets immune endocr metabol disord

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“…DDT and its metabolites have displayed harmful feminizing effects on wildlife such as birds (22,23), fish (22,24), and reptiles (22,(25)(26)(27), altering endogenous hormone levels (25,26), elevating estrogen-regulated protein levels (24), and reducing male phallus size (25,26). These reports in wildlife have led to the suggestion that organochlorines may alter a number of harmful estrogen-regulated health effects in humans such as breast cancer (1,(28)(29)(30), endometriosis (1,(31)(32)(33), spontaneous abortion (34), reduced bone mineral density (35), and decreased sperm counts (36). However, many of these reports are still controversial.…”

mentioning

confidence: 99%

DDT and its metabolites alter gene expression in human uterine cell lines through estrogen receptor-independent mechanisms.

Frigo

Burow

Mitchell

et al. 2002

Environ Health Perspect

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Endocrine-disrupting organochlorines, such as the pesticide dichlorodiphenyltrichloroethane (DDT), bind to and activate estrogen receptors (ERs), thereby eliciting estrogen-like effects. Although ERs function predominantly through activation of transcription via estrogen-responsive elements, both ERs, alpha and ss, can interact with various transcription factors such as activator protein-1 (AP-1). Additionally, estrogens may regulate early signaling events, suggesting that the biological effects of environmental estrogens may not be mediated through classic ER (alpha and ss) activity alone. We hypothesized that known environmental estrogens, such as DDT and its metabolites, activate AP-1-mediated gene transactivation through both ER-dependent and ER-independent means. Using two Ishikawa human endometrial adenocarcinoma cell line variants that we confirmed to be estrogen responsive [Ishikawa(+)] and estrogen unresponsive [Ishikawa(-)], we generated stably transfected AP-1 luciferase cell lines to identify the role of an estrogen-responsive mechanism in AP-1-mediated gene expression by various stimuli. Our results demonstrate that DDT and dichlorodiphenyldichloroethane (DDD) were the most potent activators of AP-1 activity; 2,2-bis(p-chlorophenyl) acetic acid failed to activate. Although stimulated in both Ishikawa(+) and Ishikawa(-) cells by DDT and its congeners, AP-1 activation was more pronounced in the estrogen-unresponsive Ishikawa(-) cells. In addition, DDT, DDD, and dichlorodiphenyldichloroethylene (DDE) could also stimulate AP-1 activity in the estrogen-unresponsive human embryonic kidney 293 cells using a different promoter context. Thus, our data demonstrate that DDT and its metabolites activate the AP-1 transcription factor independent of ER (alpha or ss) status.

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“…In addition to alterations of early primordial germ cell determination, gonadal differentiation, gametogenesis, development of external genitalia, various chemicals, and physical and biological conditions could affect critical signaling events regulating sexual behavior (107,(156)(157)(158)(159). These events may include male sexual behavior which is mediated in part by androgens and estrogens (160,161).…”

Section: Hypothalamic-pituitary-gonadal Axismentioning

confidence: 99%

DNA methylation and male infertility

Cisneros¹

2004

Front Biosci

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Male infertility is one of the biggest concerns of today's health care community. In the US and other developed countries, approximately 70% of infertility among couples is attributed to male reproductive failure. Alterations in reproductive organ development and sperm production have been listed as the major causes of this phenomenon. Sex determination and differentiation, X chromosome inactivation, gene imprinting and normal germ cell development are important biological processes that, in turn, control mammalian reproduction. Specific patterns of gene expression and repression are important in such processes. The strong correlation between DNA methylation, a major epigenetic modification of the genome, and gene expression patterns is well documented. The effects of DNA methylation on the expression of genes affecting male reproductive organ development, spermatogenesis, and male sexual behavior have been reported, suggesting that alterations in DNA methylation could induce abnormal male sexual development and reproductive performance. Inheritance of epigenetic processes and changes in DNA methylation patterns induced by certain diets have been demonstrated in recent years. However, the effects of DNA methylation on male fertility have not been well studied. Since inherited altered DNA methylation patterns could be a cause of increased susceptibility to xenobiotics or abnormal phenotype in future generations, multigenerational studies oriented to determine the effects of xenobiotics affecting DNA methylation in male fertility are recommended.

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Will we be taught ethics by our clones? The mutations of the living, from endocrine disruptors to genetics

Cited by 9 publications

References 0 publications

Effects of Endocrine Disruptors on Developmental and Reproductive Functions

Effects of Endocrine Disruptors on Developmental and Reproductive Functions

DDT and its metabolites alter gene expression in human uterine cell lines through estrogen receptor-independent mechanisms.

DNA methylation and male infertility

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