How mercury causes brain neuron degeneration?
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's disease 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 first 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 neurite processes at the end of each near-light is a growth cone where structural proteins are assembled to form the cell membrane.
Two principal proteins involved in growth. Cone functions are actin, which is responsible for the pulsating motion, seen here, and tubulin a major structural component of the neurite membrane during normal cell growth, tubulin molecules linked together end to end to form microtubules, which surround neural fibrils. 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 cone activity.
It is important to note that growth cones in all animal species, ranging from snails to humans, have identical structural and behavioral characteristics, and use proteins of virtually identical composition in this experiment. Neurons also isolated from snail 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 neurite membrane underwent rapid degeneration leaving behind the denuded neural fibers 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, linked together during normal cell growth, to form the microtubules which support the neurites 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 neurites microtubules begin to disassemble into free tubulin molecules, leaving the neurite stripped of its supporting structure. Ultimately, both the developing neurite and its growth cone collapse, and some denuded Nero fibrils form aggregates or tangles as depicted here shown here, is aneroid 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, the 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.