From: trigonometry1972 on
They mix the following as TR agents in meds, in
plastic to render them soft, and to render your
penis soft, your belly soft, and your brain soft.


1. Mol Cell Endocrinol. 2009 May 25;304(1-2):43-8. Epub 2009 Mar 9.

PPAR-mediated activity of phthalates:
A link to the obesity epidemic?

Desvergne B, Feige JN, Casals-Casas C.

Centre Intégratif de Génomique,
Université de Lausanne, Switzerland.
beatrice.desvergne(a)unil.ch

The endocrine disruption hypothesis asserts that exposure
to small amounts of some chemicals in the environment
may interfere with the endocrine system and lead
to harmful effects in wildlife and humans. Many of
these chemicals may interact with members of the
nuclear receptor superfamily. Peroxisome
proliferator-activatedreceptors (PPARs) are such candidate members,
which interact with many different endogenous and
exogenous lipophilic compounds. More particularly,
the roles of PPARs in lipid and carbohydrate metabolism
raise the question of their activation by a sub-class
of pollutants, tentatively named "metabolic disrupters".
Phthalates are abundant environmental micro-pollutants
in Europe and North America and may belong to this
class. Mono-ethyl-hexyl-phthalate (MEHP), a metabolite
of the widespread plasticizer di-ethyl-hexyl-phthalate
(DEHP), has been found in exposed organisms and
interacts with all three PPARs. A thorough analysis
of its interactions with PPARgamma identified MEHP
as a selective PPARgamma modulator, and thus a
possible contributor to the obesity
epidemic.

PMID: 19433246 [PubMed - indexed for MEDLINE]

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1. Philos Trans R Soc Lond B Biol Sci.
2009 Jul 27;364(1526):2047-62.

A critical analysis of the biological impacts of
plasticizers on wildlife.

Oehlmann J, Schulte-Oehlmann U, Kloas W, Jagnytsch O,
Lutz I, Kusk KO, Wollenberger L, Santos EM,
Paull GC, Van Look KJ, Tyler CR.

Department of Aquatic Ecotoxicology,
Goethe University Frankfurt am Main,
Frankfurt am Main, Germany.
oehlmann(a)bio.uni-frankfurt.de

This review provides a critical analysis of the
biological effects of the most widely used
plasticizers, including dibutyl phthalate,
diethylhexyl phthalate, dimethyl phthalate,
butyl benzyl phthalate and bisphenol A (BPA),
on wildlife, with a focus on annelids (both
aquatic and terrestrial), molluscs, crustaceans,
insects, fish and amphibians. Moreover, the paper
provides novel data on the biological effects of
some of these plasticizers in invertebrates,
fish and amphibians. Phthalates and BPA have
been shown to affect reproduction in all
studied animal groups, to impair development
in crustaceans and amphibians and to induce
genetic aberrations. Molluscs, crustaceans and
amphibians appear to be especially sensitive
to these compounds, and biological effects
are observed at environmentally relevant
exposures in the low ng l(-1) to microg l(-1)
range. In contrast, most effects in fish
(except for disturbance in spermatogenesis)
occur at higher concentrations. Most plasticizers
appear to act by interfering with the functioning
of various hormone systems, but some phthalates
have wider pathways of disruption. Effect
concentrations of plasticizers in laboratory
experiments coincide with measured environmental
concentrations, and thus there is a very real
potential for effects of these chemicals on some
wildlife populations. The most striking gaps in
our current knowledge on the impacts of plasticizers
on wildlife are the lack of data for long-term
exposures to environmentally relevant
concentrations and their ecotoxicity when
part of complex mixtures. Furthermore,
the hazard of plasticizers has been
investigated in annelids, molluscs and
arthropods only, and given the sensitivity
of some invertebrates, effects
assessments are warranted in other
invertebrate phyla.

PMID: 19528055 [PubMed - indexed for MEDLINE]

Int J Androl. 2008 Dec 16. [Epub ahead of print]

Coadministration of active phthalates results in
disruption of foetal testicular
function in rats.

Martino-Andrade AJ, Morais RN, Botelho GG,
Muller G, Grande SW, Carpentieri GB,
Leão GM, Dalsenter PR.

Departamento de Fisiologia,
Universidade Federal do Paraná,
Curitiba, Brazil.

Summary The reproductive effects of the
coadministration of di-2-(ethylhexyl)
phthalate (DEHP) and di-butyl phthalate
(DBP) were studied in both foetal and
adult male rat offspring exposed in
utero. Pregnant Wistar rats were treated by
oral gavage from gestation day 13 to
21 with vehicle control, 150 mg DEHP/kg body
weight (bw)/day, 100 mg DBP/kg bw/ or
a combination of the two compounds (DEHP
150 + DBP 100 mg/kg bw/day). An
additional group of dams received
500 mg DBP/kg bw/day. A significant
decrease in foetal testicular testosterone
levels was observed in animals exposed to
500 mg DBP/kg/day or the phthalate mixture.
Similarly, histological analysis of the
foetal testis revealed that the
coadministration of DEHP and
DBP was able to increase the diameter of
seminiferous cords and induce
gonocyte multinucleation at doses
that individually had no significant effects
on these variables. However, in the
phthalate mixture group, no significant
changes were observed in anogenital
distance and nipple retention, variables
that are used to indicate possible anti-androgenic
effects. Also, the adult endpoints investigated,
that included reproductive organ weights
and the number of spermatids per testis,
were unaffected by any treatment
regimen. Overall, coadministration of DEHP
and DBP in utero significantly reduced
testicular testosterone levels and
resulted in misshapen seminiferous
cords and gonocyte multinucleation in
rat foetal testis. Our results also confirm
that these foetal endpoints seem to be
the most sensitive markers of prenatal
phthalate exposure.

PMID: 19207615 [PubMed - as supplied by publisher]
1. Environ Health Perspect. 1982 Nov;45:77-84.

Testicular effects of phthalate esters.

Gangolli SD.

The testicular effects produced by di(2-ethylhexyl)
phthalate (DEHP) in the rat,
characterized by a decrease in the
relative organ weight and histological changes
in the seminiferous tubules, can also
be produced by di-n-butyl, di-n-pentyl and
di-n-hexyl phthalates. The corresponding
monoesters of these compounds, formed in
vivo as a result of the action of nonspecific
esterases in the intestinal mucosa
and other tissues, were equally
effective in inducing testicular damage.
Phthalate-induced testicular injury
was accompanied by a decrease in the zinc
content in the gonads and in increased
urinary excretion of this element.
Exposure of preparations of rat
seminiferous tubule cells in culture to
monophthalates capable of producing
testicular injury resulted in a dose-related
detachment of germinal cells from
Sertoli cells in a manner similar
to the effect seen in the intact animal.
This in vitro system may find application in the
elucidation of the toxic mechanisms
involved in phthalate-induced testicular
injury and in screening compounds
likely to act in a manner similar to
phthalates.

PMCID: 1568982
PMID: 6754364 [PubMed - indexed for MEDLINE]

Another gift from the establishment and also note
the date on the last abstract. They'll try to say
they had no reason to know. Sneer

This is one to be repeated until the cows come home..........Trig