re: cerebral palsy & mercury

[Guest guest]

I could have sworn I'd seen a correlation mentioned between

mercury and CP but I'll be darned if I can find it! Can anyone out

there help me with this? I've a friend whose delicate daughter has CP

and has undergone surgery after surgery. If this might help I'd sure

like to pass the information along! thanks

There is a clear connection. Cerebral palsy is a developmental

disorder that has been found to be related to environmental exposures

that affect brain development mostly prenatally. Many of the papers

reviewed in my an. bib. make it clear mercury causes the kinds of damage

known to occur in C.P. Besides my paper, I found the following 2

papers in Medline that have some relevance. Note that mercury vapor

crosses the blood brain barrier even more readily than methyl mercury,

and causes developmental effects at lower levels than MM. for some

reason, a lot of the " authorities " still prefer to focus most of the

attention on MM even though M vapor exposure occurs more commonly at

higher levels and has more developmental effects.

Bernie

Does methylmercury have a role in causing developmental

disabilities in children?

AUTHORS: Myers GJ; son PW

SOURCE: Environ Health Perspect 2000 Jun;108 Suppl 3:413-20

ABSTRACT: Methylmercury (MeHg) is a potent neurotoxin that in

high exposures can cause mental retardation, cerebral palsy, and

seizures.

Prenatal determinants of motor disorders.

AUTHORS: Stanley FJ

SOURCE: Acta Paediatr Suppl 1997

Jul;422:92-102

ABSTRACT: Cerebral palsies (CP) are the

commonest childhood motor disorders, originating in early childhood as

a result of interference in the developing brain. Identifying prenatal

factors in CP is a challenge because there is a considerable

period of time (years) between the causal event(s) and diagnosis.

Four fascinating " natural " situations provided a unique opportunity to

identify

and measure prenatal exposures in relation to motor disorders, thus

establishing the unequivocal role of some factors. However, the majority

of studies determining adverse reproductive effects of environmental

factors require a retrospective case-control approach, which present

considerable problems. Studies based on the Western Australian CP

register suggest that prenatal factors singly or in complex sequences

are more common as causes than those occurring perinatally or

postnatally.

[Guest guest]

,

Another paper on brain effects in CP and small snip from my

paper showing mercury causes exactly that kind of damage.

Bernie

Mechanisms of perinatal cerebral injury in

fetus and newborn.

AUTHORS: Delivoria-Papadopoulos M; Mishra OP

SOURCE: Ann N Y Acad Sci 2000;900:159-68

studies have shown that these enzyme

reactions

result in oxygen free radical generation, membrane

peroxidation, and cell

membrane dysfunction in the hypoxic brain.

Specifically, generation of nitric

oxide free radicals during hypoxia may lead to

nitration and nitrosylation of

specific membrane proteins and receptors, resulting in

dysfunction of receptors

and enzymes. We conclude that hypoxia-induced modification

of the NMDA

receptor leading to increased intracellular Ca2+ results in

free radical

generation and cell injury. We suggest that during hypoxia

the increased

intracellular Ca2+ may lead to increased intranuclear Ca2+

concentration and

alter nuclear events including transcription of specific

apoptotic genes and

activation of endonucleases, resulting in programmed cell

death.

*************(snip)

.. Both mercuric and methyl mercury chlorides caused dose dependent

reduction in immune B-cell production. (316) B-cell expression of IgE

receptors were significantly reduced(316,165), with a rapid and

sustained elevation in intracellular levels of calcium induced(316,333).

(316) B.J.Shenker et al, Dept. Of Pathology, Univ. Of Pennsylvania

School of Dental Medicine, " Immunotoxic effects of mercuric compounds on

human lymphocytes and monocytes: Alterations in B-cell function and

viability " Immunopharmacol Immunotoxicol, 1993, 15(1):87-112; &

J.R.Daum, " Immunotoxicology of mercury and cadmium on B-lumphocutes " , Int

J Immunopharmacol, 1993, 15(3):383-94..

(333) A.J.Freitas et al, " Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in

the rat brain " , Brain Research, 1996, 738(2): 257-64; &

P.R.Yallapragoda et al, " Inhibition of calcium transport by Hg salts " in

rat cerebellum and cerebral cortex " , J Appl toxicol, 1996, 164(4):

325-30; & E.Chavez et al, " Mitochondrial calcium release by

Hg+2 " ,J Biol Chem, 1988, 263:8, 3582-; A. Szucs et al, Cell Mol

Neurobiol, 1997,17(3): 273-8; & D.Busselberg, 1995, " Calcium channels as

target sites of heavy metals " ,Toxicol Lett, Dec;82-83:255-61; & Cell Mol

Neurobiol 1994 Dec;14(6):675-87;