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- W2461321018 abstract "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." @default.
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- W2461321018 date "2005-11-01" @default.
- W2461321018 modified "2023-09-22" @default.
- W2461321018 title "Study on oxidative function injury of Al exposure on primary cultured neuron mitochondria" @default.
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