By J. Charles Eldridge, James T. Stevens
With contributions via overseas specialists in academia, chemical production, govt examine laboratories, regulatory organizations, and personal consulting, this consultant explores the possibly destructive impression of environmental brokers at the endocrine process. It examines endocrine toxicology’s elevated value in environmental issues of safety as a result of legislative directives validated over the last ten years.
Covering all primary components of EPA difficulty, Endocrine Toxicology, 3rd Edition provides:
- putative endocrine disruptors and mechanisms of endocrine toxicity
- the historical past and standing of the regulatory process
- mechanisms of poisonous results in a number of hormonal systems
- comparisons of the endocrine responses in people, farm animals, and wildlife
- testing tools in mammalian, fish, avian, and amphibian models
- valuable perception into the techniques of assorted group of workers within the box, together with: executive officers who make and oversee coverage; scientists accountable for improvement and validation of trying out tools; simple researchers who determine poisonous mechanisms; and brands liable for environmentally benign product certification
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Additional resources for Endocrine Toxicology, Third Edition
The inclusion of multiple in vivo assays in this battery provides an opportunity to detect, with confidence, effects of both the parent compound and metabolites, as well as the comparison of potential effects in rodents (rat), fish, and amphibians. While it may be the usual case that basic endocrine functions are conserved across multiple classes of life forms, exceptions may occur. Estradiol is a dominant female hormone in mammals, fish, birds, amphibians, and reptiles, and the ER is remarkably similar across all of these vertebrate classes.
The pulsatile release of GnRH also shows a doubled pulse frequency between the infantile (15 days) and the peripubertal periods (50 days) in the male rat (47). The initiator of this increased pulsatility has sometimes been termed the “GnRH-pulse generator,” which signifies a network of neurons that are involved in the coordinated synchronous pattern in which GnRH cells discharge their products into the hypophyseal portal blood (48). Several observations suggest that this increase in frequency prior to puberty may be due to a combination of changes that take place in neuronal inputs, with “activation of excitatory” or “deactivation of inhibitory” inputs to GnRH neurons (5).
35. Owens W, Gray LE, Zeiger E, et al. The OECD program to validate the rat Hershberger bioassay to screen compounds for in vivo androgen and antiandrogen responses: phase 2 dose-response studies. Environ Health Perspect 2007; 115(5):671–678. 36. Kelce WR, Stone CR, Laws SC, et al. Persistent DDT metabolite p,p0 -DDE is a potent androgen receptor antagonist. Nature 1995; 375(6532):581–585. 37. Kelce WR, Wilson EM. Antiandrogenic effects of environmental endocrine disruptors. In: Metzler M, ed. The Handbook of Environmental Chemistry: Endocrine Disruptors, Part 1.