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Objective: 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.
Methods: 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.
Results: 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).
Conclusion: 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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