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Julio Benítez

Researcher at University of Extremadura

Publications -  108
Citations -  4483

Julio Benítez is an academic researcher from University of Extremadura. The author has contributed to research in topics: Debrisoquine & Genotype. The author has an hindex of 40, co-authored 108 publications receiving 4357 citations. Previous affiliations of Julio Benítez include University of Illinois at Urbana–Champaign & Hospital Clínico San Carlos.

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Polymorphic oxidation of debrisoquine in lung cancer patients

TL;DR: The EM phenotype of DBQ might be a secondary genetic risk factor for developing bronchogenic carcinoma in male smokers.
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Molecular analysis of the arylamine N-acetyltransferase polymorphism in a Spanish population.

TL;DR: The study of three mutations at the NAT‐2 gene locus by PCR analysis revealed that all these mutations were present in Spaniards at similar frequencies as described in other white populations, strongly contrasting with genetic differences in the CYP2D6 polymorphism between Spaniards and other white subjects.
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Polymorphic oxidation of debrisoquine in women with breast cancer.

TL;DR: Oxidative polymorphism of debrisoquine (DBQ) was determined in 98 women with breast cancer and in 446 healthy control women and might be a secondary risk factor for breast cancer in postmenopausal women.
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Modulation of CYP1A2 enzyme activity by indoleamines: inhibition by serotonin and tryptamine.

TL;DR: The occurrence of modulatory effect of 17 neurotransmitters, precursors and metabolites on the cytochrome P450 1A2 (CYP1A2) enzyme activity was studied in human liver microsomes and suggests that local activity of brain CYP1A 2 might be susceptible to local regulatory mechanisms.
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Inhibition of cytochrome P450 2C9 activity in vitro by 5-hydroxytryptamine and adrenaline.

TL;DR: The occurrence of a modulatory effect of 14 neurotransmitters, precursors and metabolites on the cytochrome P450 2C9 (CYP2C9) enzyme activity, as determined by diclofenac 4-hydroxylation, was studied in human liver microsomes and suggests that an hypothetical local activity of brain CYP2C 9 might be susceptible to regulatory mechanisms.