scholarly journals The use of a three compartment in vitro model to investigate the role of hepatic drug metabolism in drug-induced blood dyscrasias.

1993 ◽  
Vol 36 (1) ◽  
pp. 31-38 ◽  
Author(s):  
MD Tingle ◽  
BK Park
Keyword(s):  
Drug Metabolism ◽  
In Vitro Model ◽  
Hepatic Drug Metabolism ◽  
Drug Induced ◽  
Hepatic Drug ◽  
Vitro Model

scholarly journals Crypt Organoid Culture as an In Vitro Model in Drug Metabolism and Cytotoxicity Studies

2017 ◽  
Vol 45 (7) ◽  
pp. 748-754 ◽  
Author(s):  
Wenqi Lu ◽  
Eva Rettenmeier ◽  
Miles Paszek ◽  
Mei-Fei Yueh ◽  
Robert H. Tukey ◽  
...  
Keyword(s):  
Drug Metabolism ◽  
In Vitro Model ◽  
Organoid Culture ◽  
Cytotoxicity Studies ◽  
Vitro Model

Synergism between fluoxetine and the mGlu2/3 receptor agonist, LY379268, in an in vitro model for antidepressant drug-induced neurogenesis

2008 ◽  
Vol 54 (2) ◽  
pp. 428-437 ◽  
Author(s):  
F. Matrisciano ◽  
M. Zusso ◽  
I. Panaccione ◽  
B. Turriziani ◽  
A. Caruso ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
In Vitro Model ◽  
Antidepressant Drug ◽  
Drug Induced ◽  
Vitro Model

Vitamin A Status and Hepatic Drug Metabolism in the Rat

1973 ◽  
Vol 51 (1) ◽  
pp. 6-11 ◽  
Author(s):  
G. C. Becking
Keyword(s):  
Vitamin A ◽  
Drug Metabolism ◽  
Vitamin A Deficiency ◽  
Hepatic Drug Metabolism ◽  
Deficient Diet ◽  
Hepatic Drug ◽  
Vitamin A Status ◽  
Cytochrome P 450 ◽  
Liver Vitamin

The effect of vitamin A status on hepatic drug metabolism was studied in rats. Animals were fed diets with and without vitamin A for 20 and 25 days. Weight gains of control and deficient animals were not significantly different, whereas liver vitamin A levels had decreased to less than 10% of control animals after 20 days and were essentially zero after eating the deficient diet for 25 days. Aniline metabolism in vitro and aminopyrine metabolism in vitro and in vivo were significantly lower in male weanling rats fed a vitamin A deficient diet for 20 days. No alteration in in vitro p-nitrobenzoic acid metabolism was noted after 25 days on the test. Vitamin A deficiency did not alter microsomal protein levels or cytochrome c reductase activity but deficient animals did have a lower microsomal cytochrome P-450 content. Hepatic enzyme activities and cytochrome P-450 levels were restored to values approaching those found in control animals by feeding vitamin A deficient rats the vitamin A containing diet for 21 days. Liver vitamin A levels were markedly increased after re-feeding studies but were still significantly lower than control animals.

scholarly journals A Role of Intravenous Immunoglobulin in Human Parechovirus Type 3 Infection in an In Vitro Model

2016 ◽  
Vol 3 (suppl_1) ◽  
Author(s):  
Ryohei Izumita ◽  
Yuta Aizawa ◽  
Kanako Watanabe ◽  
Akihiko Saitoh
Keyword(s):  
Intravenous Immunoglobulin ◽  
In Vitro Model ◽  
Human Parechovirus ◽  
Vitro Model ◽  
Type 3

scholarly journals β-Naphthoflavone and Ethanol Reverse Mitochondrial Dysfunction in A Parkinsonian Model of Neurodegeneration

2020 ◽  
Vol 21 (11) ◽  
pp. 3955
Author(s):  
Jesus Fernandez-Abascal ◽  
Elda Chiaino ◽  
Maria Frosini ◽  
Gavin P. Davey ◽  
Massimo Valoti
Keyword(s):  
Complex I ◽  
In Vitro Model ◽  
Inhibitory Effects ◽  
Cyp Induction ◽  
Cyp Isoforms ◽  
Vitro Model ◽  
Complex I Activity ◽  
Cyp 2D6

The 1-methyl-4-phenylpyridinium (MPP+) is a parkinsonian-inducing toxin that promotes neurodegeneration of dopaminergic cells by directly targeting complex I of mitochondria. Recently, it was reported that some Cytochrome P450 (CYP) isoforms, such as CYP 2D6 or 2E1, may be involved in the development of this neurodegenerative disease. In order to study a possible role for CYP induction in neurorepair, we designed an in vitro model where undifferentiated neuroblastoma SH-SY5Y cells were treated with the CYP inducers β-naphthoflavone (βNF) and ethanol (EtOH) before and during exposure to the parkinsonian neurotoxin, MPP+. The toxic effect of MPP+ in cell viability was rescued with both βNF and EtOH treatments. We also report that this was due to a decrease in reactive oxygen species (ROS) production, restoration of mitochondrial fusion kinetics, and mitochondrial membrane potential. These treatments also protected complex I activity against the inhibitory effects caused by MPP+, suggesting a possible neuroprotective role for CYP inducers. These results bring new insights into the possible role of CYP isoenzymes in xenobiotic clearance and central nervous system homeostasis.

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