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Gandolfi A Jay
Skaggs Pharmacy Building
Primary Phone: (520) 6266696
Skaggs Pharmacy Building
1703 E. Mabel
Primary Phone: (520) 6266696
Ph.D., Oregon State University 1972
- College Of Pharmacy
A. Jay Gandolfi, PhD, is professor emeritus in the Department of Pharmacology and Toxicology and the former associate dean for research and graduate studies (1999-2012). Dr. Gandolfi taught drug disposition in both PharmD and the graduate student curricula. He directed the Graduate Council and was director of the NIEHS Superfund Program from 1999-2012.
Dr. Gandolfi's research interests were in the disposition and toxicology of drugs (e.g., anesthetics) and environmental chemicals (e.g., arsenicals) and the development of in vivo and in vitro models for studying mechanisms of toxicity.
Dr. Gandolfi joined the University of Arizona in 1978 and had appointments in the College of Medicine (Anesthesiology, Pharmacology) and the College of Pharmacy (Pharmacology and Toxicology). He received the College of Pharmacy's Findlay E. Russell MD, PhD, Distinguished Citizen Award in 2007 for services to the college and university.
Environmental Health Research & Expertise:
Dr. Gandolfi directed toxicology research projects at the University of Arizona since 1978. His research interests are in the toxicity of halogenated hydrocarbons and metals with an emphasis on hepatic and renal systems. He was also active in developing in vitro toxicity models (e.g. precision cut tissue slice culture) and the disposition of xenobiotics. He was part of the original team to coordinate and receive funding for the NIEHS Toxicology Center and was a research focus group leader from 1994 – 2012. He directed the NIEHS Superfund Program and was cofounder of the Arizona-Mexico Binational Center.
- Environmental Research Translation: Enhancing interactions with communities at contaminated sites.
- In utero and early childhood exposure to arsenic decreases lung function in children.
- Arsenic methylation capacity is associated with breast cancer in northern Mexico.
- Arsenite selectively inhibits mouse bone marrow lymphoid progenitor cell development in vivo and in vitro and suppresses humoral immunity in vivo.
- Differential binding of monomethylarsonous acid compared to arsenite and arsenic trioxide with zinc finger peptides and proteins.
- A population-based case-control study of urinary arsenic species and squamous cell carcinoma in New Hampshire, USA.
- In utero arsenic exposure and infant infection in a United States cohort: a prospective study.
- Arsenic exposure and calpain-10 polymorphisms impair the function of pancreatic beta-cells in humans: a pilot study of risk factors for T2DM.
- Exposure assessment of organochlorine pesticides, arsenic, and lead in children from the major agricultural areas in Sonora, Mexico.
- Induction of virulence factors, apoptosis, and cytokines in precision-cut hamster liver slices infected with Entamoeba histolytica.
- Metals in residential soils and cumulative risk assessment in Yaqui and Mayo agricultural valleys, northern Mexico.
- Hedgehog Signaling Regulates Bladder Cancer Growth and Tumorigenicity.
- Altered arsenic disposition in experimental nonalcoholic Fatty liver disease.
- Adjusting for Urinary Creatinine Overestimates Arsenic Concentrations in Diabetics.
- Rice consumption contributes to arsenic exposure in US women.
- Global gene expression changes in human urothelial cells exposed to low-level monomethylarsonous acid.
- Precision-cut hamster liver slices as an ex vivo model to study amoebic liver abscess.
- Monomethylarsonous acid produces irreversible events resulting in malignant transformation of a human bladder cell line following 12 weeks of low-level exposure.
- Arsenicals produce stable progressive changes in DNA methylation patterns that are linked to malignant transformation of immortalized urothelial cells.
- Mechanisms of p,p'-DDE-induced apoptosis in human peripheral blood mononuclear cells.
- Epigenetic mediated transcriptional activation of WNT5A participates in arsenical-associated malignant transformation.
- Epigenetic remodeling during arsenical-induced malignant transformation.
- Developmental and genetic modulation of arsenic biotransformation: a gene by environment interaction?
- DMPS reverts morphologic and mitochondrial damage in OK cells exposed to toxic concentrations of HgCl2.
- Mitogenic signal transduction caused by monomethylarsonous acid in human bladder cells: role in arsenic-induced carcinogenesis.
- Monomethylarsonous acid induces transformation of human bladder cells.
- Alterations in human trabecular meshwork cell homeostasis by selenium. Previous years
- Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley, Sonora, Mexico.
- Effects of arsenite on UROtsa cells: low-level arsenite causes accumulation of ubiquitinated proteins that is enhanced by reduction in cellular glutathione levels.
- Fate of effluent organic matter during soil aquifer treatment: biodegradability, chlorine reactivity and genotoxicity.
- Facile reduction of arsenate in methanogenic sludge.
- Morphologic and functional alterations induced by low doses of mercuric chloride in the kidney OK cell line: ultrastructural evidence for an apoptotic mechanism of damage.
- The metabolism of inorganic arsenic oxides, gallium arsenide, and arsine: a toxicochemical review.
- Low-level arsenite induced gene expression in HEK293 cells.
- Anaerobic biotransformation of roxarsone and related N-substituted phenylarsonic acids.
- Morphological and functional alterations in human proximal tubular cell line induced by low level inorganic arsenic: evidence for targeting of mitochondria and initiated apoptosis.
- Cold and cryopreservation of monkey liver slices.
- Anaerobic biotransformation of organo-arsenical pesticides monomethylarsonic acid and dimethylarsinic acid.
- Late administration of COX-2 inhibitors minimize hepatic necrosis in chloroform induced liver injury.
- Developmentally restricted genetic determinants of human arsenic metabolism: association between urinary methylated arsenic and CYT19 polymorphisms in children.
- Proteomic identification of ubiquitinated proteins from human cells expressing His-tagged ubiquitin.