Methylisothiazolinone et MethylChloroisothiazolinone
Une folie que nous respirons partout :
http://en.wikipedia.org/wiki/Methylisothiazolinone
http://en.wikipedia.org/wiki/Methylchlo ... iazolinone
http://leflacon.free.fr/ingredient.php?fiche=51
http://cat.inist.fr/?aModele=afficheN&cpsidt=22984570
http://leflacon.free.fr/ingredient.php?fiche=50
même sur les lingettes pour bébés :
http://www.tsr.ch/emissions/abe/1377581 ... sible.html
ne lavez pas vos bébés !!!!!
C'est plus sur !!
pour leur neurones !!
etc... sur google lisez l'horreur que on subit tous :
http://www.google.fr/search?num=100&hl= ... lisothiazo
http://www.google.fr/search?num=100&hl= ... 5&aql=&oq=
rien en Français sur wikipedia : il bouffe les neurones
Some studies have shown MIT to be allergenic and cytotoxic, and this has led to some concern over its use.[14][15] In early December, 2004, a news broadcast from WNYT in Albany, NY reported that methylisothiazolinone had been linked to nerve cell death in scientific studies. In 2002, there was an in vitro study of the neurotoxicity of MIT in the department of Neurobiology at the University of Pittsburgh.[1] In that study, it was shown that a short exposure (10 min) to concentrations of MIT of 30-100 micromolar (or 4-12 parts per million) were lethal to mature neurons in tissue culture, but not to other brain cells, such as astrocytes (support cells). The lethal actions of MIT were due to its ability to liberate the metal zinc from intracellular metal-binding sites. The liberated zinc, in turn, triggered a cell death cascade in neurons that was characterized by the sequential activation extracellular signal-regulated kinase (ERK) and NADPH oxidase. This activity led to production of reactive oxygen species (free radicals), DNA damage and the overactivation of the DNA repair enzyme poly(ADP-ribose)polymerase, or PARP. Overactivation of PARP has been linked by many investigators to cell death due to its consumption of reduced equivalents and depletion of cellular energy sources (ATP). Additional studies from the same laboratory have observed that CMIT may be significantly (30-100 times) more potent that MIT. All these studies were performed on rat brain cells in culture. A CFTA (Cosmetic, Toiletry, and Fragrance Association) response statement has come out, strongly asserting that MIT is safe in cosmetic formulas.
The CFTA response is as follows: "The abstract on Methylisothiazolinone (MI), presented at the Cell Biology 2004 meeting of the American Society for Cell Biology (ASCB) lacks a credible scientific basis in suggesting that MI could be a safety issue for consumers using personal care products. In determining the safety of any ingredient, a major factor is exposure. Cosmetic exposure is so much lower than what is presented in this abstract as to make the study meaningless for safety evaluation purposes regarding cosmetic products. The experiments conducted with MI on extracted rat nerve cells in laboratory containers do not remotely resemble the possible consumer exposure to this preservative. Reports have suggested that safety testing with animals has demonstrated that application of MI does not result in systemic toxicity to the preservative. Clinical and functional effects on the nervous system have reportedly not been observed in relevant safety tests."
The results of these safety tests have never been published in the peer-reviewed literature, nor are they easily available to the average consumer. Furthermore, the results from the abstract presented at the ASCB meeting were later published in a peer-reviewed scientific journal.[2]
The CFTA response continues: "MI is a preservative that has been specifically approved for use as a biocide by the US Environmental Protection Agency (EPA), by Japan, and by the European Commission for use in cosmetics. It is used at very low levels, parts per million (one part per million = one drop in a 55 gallon drum) in cosmetic products, including shampoos and other products. MI was reviewed by the Cosmetic Ingredient Review (CIR)* in 1992 as a component of a preservative mixture with methylchloroisothiazolinone (MCI) and found safe for use in cosmetics. Cosmetics are regulated under the Food, Drug and Cosmetic Act, which is enforced by the U.S. Food and Drug Administration (FDA). The Food and Drug Administration (FDA) has abundant legal authority to regulate the safety of cosmetic products."
A report released by the European Scientific Committee on Cosmetic Products and Non-Food Products Intended for Consumers (SCCNFP) in 2003 was of the opinion that insufficient information was available to allow for an adequate risk assessment analysis of MIT (see link below). Clearly additional studies are warranted. In 2004, after receiving additional studies, committee said "The SCCNFP is of the opinion that the proposed use of Methylisothiazolinone as a preservative at a maximum concentration of 0.01% (100 ppm) in the finished cosmetic product does not pose a risk to the health of the consumer."[3] The caveats and limitations of this conclusion are listed earlier.
Typically, methylisothiazolinone is used in products in conjunction with methylchloroisothiazolinone, this mixture is sold under the registered trade name of Kathon CG. A common indication of an allergic reaction to Kathon CG is eczema-like symptoms on the hands and wrists. These symptoms will disappear several weeks after exposure is ceased. A common point of exposure in household items is shampoos and soaps.
[edit] Physiopathological effects of MIT on developing neurons
The physiopathological effects of MIT and its closely related analog, chloromethylisothiazolinone or CMIT, reside in affecting the ability of young or developing neurons to grow processes (axons and dendrites) in tissue culture. The specific protein that is affected by MIT is called focal adhesion kinase, or FAK. Normal FAK function is required for the growth of axons and dendrites. But FAK has to be modified by a process called phosphorylation to perform its function, so phosphates are added to FAK’s amino acid chain (a process called tyrosine phosphorylation). MIT inhibits the tyrosine phosphorylation of FAK by another kinase called Src, preventing the growth of axons and dendrites, at least in culture. These findings were published in the Journal of Pharmacology and Experimental Therapeutics.[2] The toxic actions of MIT on developing neurons occurs at much lower concentrations than those inducing lethal injury (1-3 micromolar). CMIT is even more potent, working at concentrations as low as 0.1 micromolar. One micromolar is approximately
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