Copper rates, and carcass dressing percentages. Chronic copper toxicity does not normally occur in humans because of transport systems that regulate absorption and excretion. Autosomal recessive mutations in copper transport proteins can disable these systems, leading to Wilson's disease with copper accumulation and cirrhosis of the liver in persons who have inherited two defective genes. Elevated copper levels have also been linked to worsening symptoms of Alzheimer's disease. In the US, the Occupational Safety and Health Administration (OSHA) has designated a permissible exposure limit (PEL) for copper dust and fumes in the workplace as a time-weighted average (TWA) of 1 mg/m.
Mechanism of anoxic depolarization in the brain infarction, the release of glutamate and aspartate into the extracellular space causes an uncontrollable intracellular mobilization of Ca, mainly through the NMDA receptors. This is a critical stage in the development of neuronal damage, because it is the Ca overload that gives rise to several downstream cascades of events that lead to necrotic neuronal death, or to apoptosis, including free radical and nitric oxide productions that cause damage to the membrane. Another cytotoxic event that follows anoxic depolarization is lactate accumulation and acidosis as a result of glycolysis, which causes damage to the mitochondria. Ischemic insult also causes blood-brain barrier