Common shampoo ingredient stunts developing neurons of rats

[Guest guest]

Common shampoo ingredient stunts developing neurons of rats

06 Dec 2004

 

http://www.medicalnewstoday.com/medicalnews.php?newsid=17366

 

 

 

An antimicrobial agent found in many shampoos and hand lotions and widely used

in industrial settings inhibits the development of particular neuron structures

that are essential for transmitting signals between cells, according to a

University of Pittsburgh study presented today at Cell Biology 2004, the 44th

annual meeting of the American Society for Cell Biology. The meeting is being

held Dec. 4 - 8 at the Washington Convention Center.

 

Prolonged exposure to low levels of methylisothiazolinone (MIT) restricted

growth of axons and dendrites of immature rat nerve cells in culture, apparently

by disengaging the machinery of a key enzyme that is activated in response to

cell-to-cell contact, and may have potentially damaging consequences to a

developing nervous system, the researchers report.

 

" While more research is needed to determine what effect MIT would have in rodent

models, both at the cellular level and to a developing nervous system, our

results thus far suggest there is potential that everyday exposure to the

chemical could also be harmful to humans.

 

I would be particularly concerned about occupational exposure in pregnant women

and the possibility of risk to the fetus, " said senior author Elias Aizenman,

Ph.D., professor of neurobiology at the University of Pittsburgh School of

Medicine.

 

Dr. Aizenman became interested in MIT as an offshoot to his primary area of

research on the mechanisms of neuronal cell death. The first he heard of the

chemical was when its name came up in a literature search for compounds with

specific chemical properties that he thought would incite a particular cell

death pathway he recently had identified.

 

As it turned out, MIT activated a different, novel pathway, but Dr. Aizenman

remained intrigued, in large part because of the considerable lack of scientific

data about a compound that he came to realize was listed on numerous consumer

product labels and was very widely used in industry.

 

As an antimicrobial agent, or biocide, MIT and related compounds kill harmful

bacteria that like to grow near moisture or water. As such, they often are found

in personal care products, as well as in water-cooling systems and at factories

that require water for manufacturing. Since learning about MIT, Dr. Aizenman has

not found any published neurotoxicity reports, or concrete data in any public

documents filed with the Environmental Protection Agency.

 

The first set of studies he and his team published in 2002 in The Journal of

Neuroscience involved acute exposure to mature rat neurons. They reported that

10-minute exposure at a high concentration - roughly 100 times the dose used in

their current study - was lethal to these cells.

 

To understand what effect chronic exposure would have on immature, developing

neurons, the researchers kept cells in a media solution containing low

concentrations of MIT for 18 hours.

 

In a standard culture, an immature neuron will in such time develop an axon, the

extension from the cell body used for sending signals to other cells, and

several dendrites, elaborate projections that receive incoming information. But

after exposure to MIT, the cells had few, if any, axons and dendrites, with the

inhibition of their growth being dose-dependent, reported Kai He, Ph.D., a

postdoctoral fellow working with Dr. Aizenman who presented the data at Cell

Biology 2004.

 

Additional studies revealed that MIT significantly hindered tyrosine

phosphorylation, a process that initiates molecular events during cell-to-cell

contact, and that a particular protein enzyme was its target. This enzyme, focal

adhesion kinase (FAK), is known to be important for outgrowth of axons and

dendrites as well as necessary for cell signaling.

 

But to kick into action, FAK must undergo tyrosine phosphorylation, whereby

collections of molecules called phosphate groups are added to FAK's sequence of

amino acids.

 

Like all proteins, FAK is comprised of a unique sequence of some 20 amino acids,

including tyrosine, so any change, such as through phosphorylation, essentially

changes its function. To pinpoint the exact site along FAK's sequence where

tyrosine phosphorylation was being inhibited, the researchers had to determine

which of its tyrosines were targeted by MIT. Digging further, they found that

one tyrosine in particular (amino acid 576 in the protein sequence) was more

substantially affected by MIT, an indication that this particular amino acid

residue is important for axon and dendrite growth and development.

 

" Since we know FAK to be highly expressed in the nerve tissue during brain

development, this study suggests that phosphorylation of tyrosine 576 may be

critical for axon and dendrite outgrowth, " Dr. He reported.

 

The authors, who also included Carl F. Lagenaur, Ph.D., associate professor of

neurobiology at the University of Pittsburgh School of Medicine, plan additional

research to further understand the molecular mechanisms underlying MIT's

neurotoxic effect on cells, as well as studies involving whole animals. They are

hopeful that their work will stimulate additional research by other groups as

well as bring heightened awareness about the potential risks from human

exposure.

 

" This chemical is being used more and more extensively, yet there have been no

neurotoxicity studies in humans to indicate what kind and at what level exposure

is safe. I realize it's a big leap to suggest there may be a parallel between

environmental exposure and the noticeably higher rates of diagnosed childhood

developmental disabilities, but I would caution that based on our data, there

very well could be neurodevelopmental consequences from MIT. Clearly, more study

is needed, with both scientists and government regulators equally engaged, "

added Dr. Aizenman.

 

NOTE TO EDITORS: This abstract, Lack of Phosphorylation of Tyrosine 576 of Focal

Adhesion Kinase Correlates to Neurite Outgrowth Deficiency Following

Methylisothiazolinone Treatment in Cultured Cortical Neurons (Poster

Presentation 300), is being presented at 1:30 p.m., Sunday, Dec. 5 in Session

123 Focal Adhesions. To arrange interviews with the authors, please call Lisa

Rossi at 412-916-3315 (cell). The press contact for the American Society for

Cell Biology (ASCB) is John Fleischman, who can be reached at

jfleischman or at 202-249-4019 between Dec. 4 - 8. The ASCB Newsroom is

located in Room 101 of the Washington Convention Center.

 

Contact: Lisa Rossi

RossiL

(Cell - 412-916-3315)

Phone: 412-647-3555

Fax: 412-624-3184

 

Craig Dunhoff

DunhoffCC

Phone: 412-647-3555

Fax: 412-624-3184

University of Pittsburgh Medical Center

_________________

 

JoAnn Guest

mrsjoguest

DietaryTipsForHBP

www.geocities.com/mrsjoguest/Genes

 

 

 

 

 

AIM Barleygreen

" Wisdom of the Past, Food of the Future "

 

http://www.geocities.com/mrsjoguest/Diets.html