Teratogenesis birth defects

However, most public concern does not center around death or other acute intoxication symptoms, but rather those chronic injuries which we term as irreversible. These are carcinogenesis (cancer), teratogenesis (birth defects), or mutagenesis (genetic defects). There have been three good studies involving the ability of 2,4-D to cause cancer. The conclusion by the authors of these three studies is that there is no evidence that 2,4-D causes cancer. However, the study design was such that they were not adequate to prove that 2,4-D could not cause cancer, and as a result, further cancer studies were required by the EPA which should provide a definitive answer. 

Handley-Goldstone HM, Grow MW, Stegeman JJ (2005) Cardiovascular gene expression profiles of dioxin exposure in zebrafish embryos. Toxicol Sci 85 683-693 Hansen JM (2006) Oxidative stress as a mechanism of teratogenesis. Birth Defects Res Part C Embryo Today Rev 78 293-307... 

Reproductive Toxicology (mammalian) The study of the effects of chemicals on the adult reproductive and neuroendocrine systems, the embryo, foetus, neonate and prepubertal mammal. Reproductive Toxins Tire tenn refers to a specific target organ characterization of effect. These are chemicals which affect the reproductive capabilities including chromosomal damage (mutations) and effects on fetuses (teratogenesis). Signs and symptoms include birth defects sterility. Examples are lead and DBCP. 

Teratogenesis Defects in embryonic and foetal development caused by a substance. Teratogenic capable of producing birth defects. 

When one compares the risk of caffeine as taken in one cup of coffee to that from the forest herbicide, 2,4-D, one finds that the margin of safety for teratogenesis or birth defects ranges from 5 to 16 (Table XIII). 

Ingestion. Teratogenesis (triggers birth defects), fetal toxicity, liver and kidney damage, cancer, brittle hair and nails, skin lesions, some effects on central, peripheral nervous systems. Selenosis. 

Ethionine-induced teratogenesis has been reported in rats and chicks. Both mice and rats demonstrate significant strain difference to the carcinogenic effects that are caused by ethionine. In addition to cancer, the ethionine-induced abnormal methylation may also have pathological effects leading to birth defects, neurological disorder, and liver and pancreatic toxicities. 

Approximately 7% of all live-born humans bear birth defects. This value may be as high as 10% if children are evaluated to age 10 years to include subtle structural or functional deficits such as minimal brain dysfunction or attention deficit disorders. More than 560 000 lives out of 3 million births per year in the United States are lost through infant death, spontaneous abortion, stillbirths, and miscarriage due presumably to defective fetal development. The relative contributions to human teratogenesis have been estimated as follows known germinal mutations, 20% chromosomal and gene aberrations, 3-5% environmental causes such as radiation, <1% infections, 2% or 3% maternal metabolic imbalance, 1% or 2% drugs and environmental chemicals, 4% or 5% contributions from maternal dietary deficiencies or excesses and... 

Teratogens are chemical species that canse birth defects. These usually arise from damage to embryonic or fetal cells. However, mntations in germ cells (egg or sperm cells) may canse birth defects, snch as Down s syndrome. The biochemical mechanisms of teratogenesis are varied. These include enzyme inhibition by xenobiotics deprivation of the fetus of essential substrates, such as vitamins interference with energy supply or alteration of the permeability of the placental membrane. 

TERATOGENIC Causing birth defects comes from the Greek word teratogenesis, meaning monster-making. ... 

The ability of a xenobiotic to bind reversibly to a receptor does not preclude its being bioactivated to a reactive intermediate, or vice versa (Fig. 5). Similarly, for some birth defects, both mechanisms potentially could contribute to the same teratological outcome, and different mechanisms may predominate in different strains and species at different gestational times of pregnancy, or in different embryonic-fetal target tissues or cell t3 pes. These possibilities often confound a precise elucidation of the mechanism of teratogenesis for a given xenobiotic. 

Oxidative DNA damage and repair in teratogenesis and neurodevelopmental deficits. Birth Defects Res C Embryo Today. Vol. 90 No. 2 pp. 103-109 ISSN 1542-9768 Yukawa, M., Oda, S., Mitani, H., Nagata, M. and Aoki, F. (2007). Deficiency in the response to DNA double-strand breaks in mouse early preimplantation embryos. Biochem Biophys Res Commun. Vol. 358 No. 2 pp. 578-584 ISSN 0006-291X Zhao, T. and Xu, Y. (2010). p53 and stem cells new developments and new concerns. Trends Cell Biol. Vol. 20 No. 3 pp. 170-175 ISSN 1879-3088... 

Since the piperidines behave in a specific way and are teratogenic, they also fulfill specific criteria for teratogenesis [23, 24, 38, 70, 85]. The structural characteristics of these piperidines need to be determined and their main differences outlined to be able to find out their mechanism of action, as fetal movement and malpositioning. The birth defects caused by Conium maculatum are the same, and their biological activities occur by a similar mechanism of action [16,52, 65,66,70]. As usual with biological active compounds one use to characterize the toxicity into acute and chronic forms. The peripheral actions of coniine are similar to those of nicotine, but it produces more pronounced paralysis of the central nervous system and of the skeletal muscle nerve [65, 70]. 

Another virtual tissue model being developed is the v-embryo. This simulation investigates teratogenesis, or the production of birth defects, resulting from chemical exposures in a pregnant woman. The model is being constructed largely from zebrafish... 

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