Abstract:
:It has been reported that lead could induce apoptosis in a variety of cell types. Although mitochondrion is regarded as the most pertinent pathway in mediating apoptosis, the exact mechanisms of lead-induced apoptosis are still largely unknown. Furthermore, there is little information about expressions and regulations of Bax, Bcl-2, and p53 in lead-induced apoptosis, which are critical regulators of mitochondrial stability. The present study was undertaken to determine whether lead could induce DNA damage and apoptosis in PC 12 cells, and the involvement of Bax, Bcl-2, p53, and caspase-3 in this process. The results showed that lead could induce DNA damage and apoptosis in PC 12 cells, accompanying with upregulation of Bax and downregulation of Bcl-2. Additionally, the expression of p53 increased, and caspase-3 was activated. Therefore, it suggests that lead can induce activation of p53 by DNA damage, which may lead to imbalance of Bax/Bcl-2 and mitochondrial dysfunction. Subsequently, after activation of caspase-3, lead-induced apoptosis occurres.
journal_name
Toxicol Lettjournal_title
Toxicology lettersauthors
Xu J,Ji LD,Xu LHdoi
10.1016/j.toxlet.2006.06.643subject
Has Abstractpub_date
2006-10-10 00:00:00pages
160-7issue
2eissn
0378-4274issn
1879-3169pii
S0378-4274(06)00844-7journal_volume
166pub_type
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