Aluminum-induced apoptosis in PC12D cells.
The addition of aluminum-maltol complex to PC12D cells induced a time-dependent and concentration-dependent growth inhibition as well as cell death, whereas aluminum chloride or maltol alone did not affect the viability of PC12D cells. Apoptosis of differentiated PC12D cells was assessed by using terminal deoxynucleotidyltransferase-mediated 2'-deoxyuridine-5'-triphosphate nick end labeling (TUNEL) technique to detect DNA strand breaks in situ. The number of TUNEL-positive cells treated with aluminum-maltol increased with time in the treatment cultures. The ability of aluminum ion to elevate intracellular reactive oxygen species was determined by fluorescence in PC12D cells loaded with the oxidant-sensitive dye 2',7'-dichlorofluorescin diacetate. Aluminum ion incorporated to PC 12D cells causes apoptotic cell death by enhancing the generation of reactive oxygen species.
Tsubouchi
R
R
Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Japan.
Htay
H H
HH
Murakami
K
K
Haneda
M
M
Yoshino
M
M
D000535:Aluminum / Q000009:adverse effects / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D006801:Humans; D020287:In Situ Nick-End Labeling; D020932:Nerve Growth Factor / Q000494:pharmacology; D016716:PC12 Cells; D011753:Pyrones / Q000494:pharmacology*; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013997:Time Factors
D011753:Pyrones; D017382:Reactive Oxygen Species; C008316:maltol; D020932:Nerve Growth Factor; D000535:Aluminum