How mercury causes brain neuron degeneration – F.L Lorsheider, C.CW Leong, N.I Syed

Dept. of physiology and biophysics, faculty of medicine, University of Calgary.

Mercury has long been known to be a potent neurotoxin substance whether it is inhaled or consumed in the diet as a food contaminant over the past 15 years medical research laboratories have established that dental amalgam tooth fillings are a major contributor to mercury body burden.

In 1997 a team of research scientists demonstrated that mercury vapor inhalation by animals produced a molecular lesion in brain protein metabolism which was similar to a lesion seen in 80% of Alzheimer diseased brains.

Recently completed experiments by scientists at the University of Calgary’s Faculty of Medicine now reveal with direct visual evidence from brain neuron tissue cultures how mercury ions actually alter the cell membrane structure of developing neurons.

To better understand Mercury’s effect on the brain let us illustrate what brain neurons look like and how they grow.

In this animation we see three brain neurons growing in tissue culture, each with a central cell body and numerous and neurite processes.

At the end of each neurite, there is a growth cone where structural proteins are assembled to form the cell membrane.

Two principle proteins involved in growth cone function are actin which is responsible for the pulsating motion seen here and tubulin – a major structural component of neuron membrane

During normal cell growth, tubulin molecules are linked together end to end to form microtubules that surround neural fibers - another structural protein component of the neuronal axon.

Shown here is the neurite of a live neuron isolated from snail brain tissue displaying linear growth due to growth con activity. It is important to note that growth cones in all animal species ranging from snail to humans have identical structural and behavioral characteristics and use proteins of virtually identical composition.

In this experiment neurons also isolated from small brain tissue were grown in culture for several days after which very low concentrations of mercury were added to the culture medium for 20 minutes.

Over the next 30 minutes the neuroid membrane underwent rapid degeneration, leaving behind the denuded Nero Fibrils seen here.

In contrast other heavy metals added this same concentration such as aluminum lead cadmium and manganese did not produce this effect.

To understand how mercury causes this degeneration, let us return to our illustration as mentioned before tubulin proteins are linked together during normal cell growth to form the microtubules which support the neurite structure.

When mercury ions are introduced into the culture medium they infiltrate the cell and bind themselves to newly synthesized tubulin molecules more specifically the mercury ions attach themselves to the binding site reserved for guanosine triphosphate or GTP on the beta subunit of the affected tubulin molecules.

Since bound GTP normally provides the energy which allows tubulin molecules to attach to one another. Mercury ions bound to these sites prevent tubulin proteins from linking together, consequently, the neuritis microtubules begin to disassemble into free tubulin molecules living the nur/light stripped of its supporting structure. Ultimately both the developing neurite and its growth cone collapse and some denuded neuro-fibromas from aggregates or tangles as depicted here.

Shown here is a neuroid growth cone stained specifically for tubulin and actin before and after mercury exposure. Note that the mercury has caused the disintegration of the tubulin microtubule structure. These new findings reveal important visual evidence as to how mercury causes Neurodegeneration.

More importantly, this study provides the first direct evidence that low-level mercury exposure is indeed a precipitating factor that can initiate this narrow degenerative process within the brain.