Transgenesis of the Aldehyde Dehydrogenase-2 (ALDH2) Locus in a Mouse Model and in Cultured Human Cells

1995 ◽  
pp. 131-136 ◽  
Author(s):  
Cheng Chang ◽  
Jerry Mann ◽  
Akira Yoshida
Keyword(s):  
Mouse Model ◽  
Aldehyde Dehydrogenase ◽  
Human Cells ◽  
Aldehyde Dehydrogenase 2 ◽  
Cultured Human Cells

Disruption of the aldehyde dehydrogenase 2 gene increases the bone anabolic response to intermittent PTH treatment in an ovariectomized mouse model

Bone ◽  
2020 ◽  
Vol 136 ◽  
pp. 115370
Author(s):  
Kenji Kosugi ◽  
Takafumi Tajima ◽  
Kunitaka Menuki ◽  
Kayoko Furukawa Okuma ◽  
Kotaro Tokuda ◽  
...  
Keyword(s):  
Mouse Model ◽  
Aldehyde Dehydrogenase ◽  
Aldehyde Dehydrogenase 2 ◽  
Anabolic Response ◽  
Ovariectomized Mouse ◽  
Aldehyde Dehydrogenase 2 Gene ◽  
Intermittent Pth

Alpha-Tocopherol Protects Cultured Human Cells from the Acute Lethal Cytotoxicity of Dioxin

2002 ◽  
Vol 72 (3) ◽  
pp. 147-153 ◽  
Author(s):  
Kei-Ichi Hirai ◽  
Jie-Hong Pan ◽  
Ying-Bo Shui ◽  
Eriko Simamura ◽  
Hiroki Shimada ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Damage ◽  
Smooth Endoplasmic Reticulum ◽  
Dehydroascorbic Acid ◽  
Human Cells ◽  
Alpha Tocopherol ◽  
Cervical Cancer Cells ◽  
Cultured Human Cells ◽  
Nuclear Damage ◽  
Conjunctival Epithelial Cells

The possible protection of cultured human cells from acute dioxin injury by antioxidants was investigated. The most potent dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), caused vacuolization of the smooth endoplasmic reticulum and Golgi apparatus in cultured human conjunctival epithelial cells and cervical cancer cells. Subsequent nuclear damage included a deep irregular indentation resulting in cell death. A dosage of 30–40 ng/mL TCDD induced maximal intracellular production of H2O2 at 30 minutes and led to severe cell death (0–31% survival) at two hours. A dose of 1.7 mM alpha-tocopherol or 1 mM L-dehydroascorbic acid significantly protected human cells against acute TCDD injuries (78–97% survivals), but vitamin C did not provide this protection. These results indicate that accidental exposure to fatal doses of TCDD causes cytoplasmic free radical production within the smooth endoplasmic reticular systems, resulting in severe cytotoxicity, and that vitamin E and dehydroascorbic acid can protect against TCDD-induced cell damage.

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