PMID: 16535836Mar 16, 2006Paper

Study on oxidative function injury of Al exposure on primary cultured neuron mitochondria

Wei sheng yan jiu = Journal of hygiene research
S HeSheng Wang

Abstract

To study the possible mechanism of Al neurotoxicity, we evaluated the oxidative function injury of mitochondria in the primary cultured neurons that were exposed to various concentrations of AlCl3. Neurons from newborn SD rats were primarily cultured. Then they were exposed to AlCl3 of 0 micromol/L, 50 micromol/L, 100 micromol/L, and 500 micromol/L. The neuron death rate, mitochondria enzyme activity, mitochondria reactive oxygen species (ROS) and mitochondria membrane potential (MMP) were tested then. When the concentration of AlCl3 increased (0 micromol/L, 50 micromol/L, 100 micromol/L, 500 micromol/L), the death rate increased (10.53%, 11.99%, 12.03%, 25.00%), mitochondria enzyme activity decreased (0.56, 0.47, 0.42, 0.32), ROS increased (17.12, 19.71, 29.67, 45.46) and MMP decreased(8.03, 8.02, 4.69, 3.01). Al exposure could cause mitochondria oxidative function injury in the primarily cultured rats, which may be the one of the possible mechanism of Al toxicity.

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