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Copper toxicity

Copper toxicity damages mitochondria of brain cells through oxidative, nitrosative stress

Monday, February 03, 2014 by: David Gutierrez, staff writer
Tags: copper toxicity, brain cells, oxidative stress

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(NaturalNews) Scientists have linked copper to the development of numerous brain disorders, including Alzheimer's disease, prion conditions such as mad cow disease, and Wilson's disease. Although it remains unclear exactly what role copper plays in such brain damage, at least one study suggests that the mineral's oxidative properties may be partly to blame.

Copper is a trace mineral that is essential for health in small quantities. In appropriate amounts, it is critical for the health of bones, red blood cells, blood vessels, nerves and the immune system. In higher doses, however, it is known to act as a neurotoxin.

The study was conducted by researchers from the University of Miami and published in the journal Laboratory Investigation in 2008. The researchers exposed two different types of brain cells, astrocytes and neurons, to copper and then examined the cells to see if the permeability of their mitochondria had been impaired.

Most of the damage observed occurred in astrocytes, rather than neurons. While neurons are the brain cells that transmit messages, astrocytes are actually the most common cells in the brain. They play many critical roles, including repairing brain damage and scarring and supporting the health of the blood-brain barrier, which keeps toxins out of the brain.

The researchers found that 12 hours after copper exposure, astrocytes underwent a 36 percent reduction in the inner mitochondrial membrane potential (Delta Psi m), a marker of the mitochondrial permeability transition (mPT). 24 hours after copper exposure, Delta Psi m had been reduced by 48 percent, and it did not recover for at least 72 hours. Cobalt quenching of calcein fluorescence, another marker of mPT, decreased by 45 percent within 24 hours of copper exposure.

Notably, nearly all this damage was prevented when the astrocytes were pre-treated with antioxidants. This suggests that many of the changes observed were due to oxidative damage.

Antioxidants prevent brain cell death

The researchers also found that, 24 hours after exposure, astrocytes had 30 percent lower levels of the energy-transporting chemical ATP. This effect was completely blocked, however, when the astrocytes were treated with the drug cyclosporin A (CsA).

CsA is an immunosuppressant drug that has recently been investigated for the ability to protect the nervous system in cases of traumatic brain injury. Studies suggest that the drug prevents the formation of mPT pores, which have been linked to brain damage in cases of both injury and neurodegenerative disease.

Finally, copper exposure actually killed 42 percent of astrocytes within 48 hours. CsA reduced this mortality by 41 percent, while antioxidants reduced it by between 35 and 60 percent.

While neurons did not experience mPT in response to copper exposure the way that astrocytes did, they still tended to die upon exposure. In addition, their ATP levels were reduced 63 percent within 14 hours of exposure. CsA had no effect in protecting neurons from copper-induced mortality, but antioxidants and drugs known as nitric oxide synthase inhibitors were successful in doing so.

Finally, protein tyrosine nitration - an effect similar to oxidation, but caused by nitrogen-containing compounds instead of oxygen-containing ones - increased in both astrocytes and neurons upon copper exposure

"These studies indicate that mPT, and oxidative and nitrosative stress represent major factors in copper-induced toxicity in astrocytes," the researchers wrote, "whereas oxidative and nitrosative stress appears to play a major role in neuronal injury."

Another recent study, conducted by researchers from the University of Rochester, found that copper may increase the risk of Alzheimer's disease even at exposure levels found in the normal U.S. diet. They found that copper damaged the blood-brain barrier, induced inflammation and accelerated the buildup of toxic amyloid-beta proteins.

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