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822 results on '"Pogribny, Igor"'

110. Moderate folate depletion increases plasma homocysteine and decreases lymphocyte DNA methylation in postmenopausal women

Author

Jacob, Robert A., Gretz, Denise M., Taylor, Peter C., James, S. Jill, Pogribny, Igor P., Miller, Barbara J., Henning, Susanne M., and Swendseid, Marian A.

Subjects
Postmenopausal women -- Food and nutrition, Folic acid in human nutrition -- Research, Methylation -- Research, Food/cooking/nutrition
Abstract

To determine the human folate requirement on the basis of changes in biochemical pathways, we studied the effect of controlled folate intakes on plasma homocysteine and lymphocyte DNA methylation and deoxynucleotide content in healthy postmenopausal women. Eight women (49-63 y of age) were housed in a metabolic unit and fed a low folate diet containing 56 [[micro]gram]/d of folate for 91 d. Folate intake was varied by supplementing 55-460/[[micro]gram]/d of folic acid (pteroylglutamic acid) to the diet to provide total folate intake periods of 5 wk at 56 [[micro]gram]/d, 4 wk at 111 [[micro]gram]/d and 3 wk at 286-516 [[micro]gram]/d. A subclinical folate deficiency with decreased plasma folate was created during the first two periods. This resulted in significantly elevated plasma homocysteine and urinary malondialdehyde, and lymphocyte DNA hypomethylation. The folate depletion also resulted in an increased ratio of dUTP/dTTP in mitogen-stimulated lymphocyte DNA and decreased lymphocyte NAD, changes suggesting misincorporation of uracil into DNA and increased DNA repair activity. The DNA hypomethylation was reversed with 286-516 [[micro]gram]/d of folate repletion, whereas the elevated homocysteine decreased with 516 but not 286 [[micro]gram]/d of folate. The results indicate that marginal folate deficiency may alter DNA composition and that the current RDA of 180 [[micro]gram]/d may not be sufficient to maintain low plasma homocysteine concentrations of some postmenopausal women. KEY WORDS: folic acid; homocysteine; methylation; DNA; humans

Published
1998

117. Carcinogenicity of isobutyl nitrite, beta-picoline, and some acrylates

Author

Kromhout, Hans, Friesen, Melissa, Marques, M. Mathilde, Sergi, Consolato Maria, Abdallah, Mohamed, Benke, Geza, Cesta, Mark, Germolec, Dori, Houck, Keith, Ichihara, Gaku, Jameson, Charles William, Kanno, Jun, Pogribny, Igor, Svendsen, Camilla, Benbrahim-Tallaa, Lamia, Guyton, Kathryn Z., Grosse, Yann, El Ghissassi, Fatiha, Bouvard, Veronique, Hall, Amy, Jaillet, Corentin, Mattock, Heidi, Straif, Kurt, One Health Chemisch, and dIRAS RA-2

Published
2018

119. Gene Expression and DNA Methylation Alterations in the Glycine N-Methyltransferase Gene in Diet-Induced Nonalcoholic Fatty Liver Disease-Associated Carcinogenesis

Author

Borowa-Mazgaj, Barbara, primary, de Conti, Aline, additional, Tryndyak, Volodymyr, additional, Steward, Colleen R, additional, Jimenez, Leandro, additional, Melnyk, Stepan, additional, Seneshaw, Mulugeta, additional, Mirshahi, Faridodin, additional, Rusyn, Ivan, additional, Beland, Frederick A, additional, Sanyal, Arun J, additional, and Pogribny, Igor P, additional

Published
2019
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120. Population-Based Analysis of DNA Damage and Epigenetic Effects of 1,3-Butadiene in the Mouse

Author

Lewis, Lauren, primary, Borowa-Mazgaj, Barbara, additional, de Conti, Aline, additional, Chappell, Grace A., additional, Luo, Yu-Syuan, additional, Bodnar, Wanda, additional, Konganti, Kranti, additional, Wright, Fred A., additional, Threadgill, David W., additional, Chiu, Weihsueh A., additional, Pogribny, Igor P., additional, and Rusyn, Ivan, additional

Published
2019
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123. Histopathological and Molecular Signatures of a Mouse Model of Acute-on-Chronic Alcoholic Liver Injury Demonstrate Concordance With Human Alcoholic Hepatitis

Author

Furuya, Shinji, primary, Cichocki, Joseph A, additional, Konganti, Kranti, additional, Dreval, Kostiantyn, additional, Uehara, Takeki, additional, Katou, Yuuki, additional, Fukushima, Hisataka, additional, Kono, Hiroshi, additional, Pogribny, Igor P, additional, Argemi, Josepmaria, additional, Bataller, Ramon, additional, and Rusyn, Ivan, additional

Published
2018
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124. Folate deficiency in rats induces DNA strand breaks and hypomethylation within the p53 tumor suppressor gene

Author

Kim, Young-In, Pogribny, Igor P., Basnakian, Alexi G., Miller, Joshua W., Selhub, Jacob, James, S. Jill, and Mason, Joel B.

Subjects
Folic acid deficiency -- Complications, DNA damage -- Causes of, Carcinogenesis -- Causes of, Tumor suppressor genes -- Abnormalities, Food/cooking/nutrition, Health
Abstract

Folate is essential for the de novo biosynthesis of purines and thymidylate, and is an important mediator in the transfer of methyl groups for DNA methylation. Folate deficiency, therefore, could contribute to abnormal DNA integrity and methylation patterns. We investigated the effect of isolated folate deficiency in rats on DNA methylation and DNA strand breaks both at the genomic level and within specific sequences of the p53 tumor suppressor gene. Our data indicate that folate deficiency induces DNA strand breaks and hypomethylation within the p53 gene. Such alterations either did not occur or were chronologically delayed when examined on a genome-wide basis, indicating some selectivity for the exons examined within the p53 gene. Folate insufficiency has been implicated in the development of several human and experimental cancers, and aberrations within these regions of the p53 gene that were examined in this study are thought to play an integral role in carcinogenesis. The aforementioned molecular alterations may therefore be a means by which dietary folate deficiency enhances carcinogenesis.

Published
1997

125. Carcinogenicity of isobutyl nitrite, beta-picoline, and some acrylates

Author

One Health Chemisch, dIRAS RA-2, Kromhout, Hans, Friesen, Melissa, Marques, M. Mathilde, Sergi, Consolato Maria, Abdallah, Mohamed, Benke, Geza, Cesta, Mark, Germolec, Dori, Houck, Keith, Ichihara, Gaku, Jameson, Charles William, Kanno, Jun, Pogribny, Igor, Svendsen, Camilla, Benbrahim-Tallaa, Lamia, Guyton, Kathryn Z., Grosse, Yann, El Ghissassi, Fatiha, Bouvard, Veronique, Hall, Amy, Jaillet, Corentin, Mattock, Heidi, Straif, Kurt, One Health Chemisch, dIRAS RA-2, Kromhout, Hans, Friesen, Melissa, Marques, M. Mathilde, Sergi, Consolato Maria, Abdallah, Mohamed, Benke, Geza, Cesta, Mark, Germolec, Dori, Houck, Keith, Ichihara, Gaku, Jameson, Charles William, Kanno, Jun, Pogribny, Igor, Svendsen, Camilla, Benbrahim-Tallaa, Lamia, Guyton, Kathryn Z., Grosse, Yann, El Ghissassi, Fatiha, Bouvard, Veronique, Hall, Amy, Jaillet, Corentin, Mattock, Heidi, and Straif, Kurt

Published
2018

128. Carcinogenicity of isobutyl nitrite, β-picoline, and some acrylates

Author

Kromhout, Hans, primary, Friesen, Melissa, additional, Marques, M Mathilde, additional, Sergi, Consolato Maria, additional, Abdallah, Mohamed, additional, Benke, Geza, additional, Cesta, Mark, additional, Germolec, Dori, additional, Houck, Keith, additional, Ichihara, Gaku, additional, Jameson, Charles William, additional, Kanno, Jun, additional, Pogribny, Igor, additional, Svendsen, Camilla, additional, Benbrahim-Tallaa, Lamia, additional, Guyton, Kathryn Z, additional, Grosse, Yann, additional, El Ghissassi, Fatiha, additional, Bouvard, Véronique, additional, Hall, Amy, additional, Jaillet, Corentin, additional, Mattock, Heidi, additional, Straif, Kurt, additional, Kromhout, Hans, additional, Marques, M. Matilde, additional, Cesta, Mark F., additional, and Guyton, Kathryn, additional

Published
2018
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132. Epigenetically mediated inhibition of S‐adenosylhomocysteine hydrolase and the associated dysregulation of 1‐carbon metabolism in nonalcoholic steatohepatitis and hepatocellular carcinoma

Author

Pogribny, Igor P., primary, Dreval, Kostiantyn, additional, Kindrat, Iryna, additional, Melnyk, Stepan, additional, Jimenez, Leandro, additional, Conti, Aline, additional, Tryndyak, Volodymyr, additional, Pogribna, Marta, additional, Ortega, Juliana Festa, additional, James, S. Jill, additional, Rusyn, Ivan, additional, and Beland, Frederick A., additional

Published
2018
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135. Drug, herb, and dietary supplement hepatotoxicity

Author

Pogribny, Igor P., Teschke, Rolf, Andrade, Raul J., Pogribny, Igor P., Teschke, Rolf, and Andrade, Raul J.

Abstract

The past decade has witnessed drugs, herbs, and dietary supplements share the common feature of potential liver injury in a few susceptible individuals...

Published
2017

137. Multiple microRNAs function as self-protective modules in acetaminophen-induced hepatotoxicity in humans

Author

Yu, Dianke, primary, Wu, Leihong, additional, Gill, Pritmohinder, additional, Tolleson, William H., additional, Chen, Si, additional, Sun, Jinchun, additional, Knox, Bridgett, additional, Jin, Yaqiong, additional, Xiao, Wenming, additional, Hong, Huixiao, additional, Wang, Yong, additional, Ren, Zhen, additional, Guo, Lei, additional, Mei, Nan, additional, Guo, Yongli, additional, Yang, Xi, additional, Shi, Leming, additional, Chen, Yinting, additional, Zeng, Linjuan, additional, Dreval, Kostiantyn, additional, Tryndyak, Volodymyr, additional, Pogribny, Igor, additional, Fang, Hong, additional, Shi, Tieliu, additional, McCullough, Sandra, additional, Bhattacharyya, Sudeepa, additional, Schnackenberg, Laura, additional, Mattes, William, additional, Beger, Richard D., additional, James, Laura, additional, Tong, Weida, additional, and Ning, Baitang, additional

Published
2017
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142. Chemo brain or tumor brain - that is the question: the presence of extracranial tumors profoundly affects molecular processes in the prefrontal cortex of TumorGraft mice

Author

Kovalchuk, Anna, primary, Ilnytskyy, Yaroslav, additional, Rodriguez-Juarez, Rocio, additional, Shpyleva, Svitlana, additional, Melnyk, Stepan, additional, Pogribny, Igor, additional, Katz, Amanda, additional, Sidransky, David, additional, Kovalchuk, Olga, additional, and Kolb, Bryan, additional

Published
2017
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149. Opportunities to integrate new approaches in genetic toxicology: An ILSI-HESI workshop report

Author

Zeiger, Errol, Gollapudi, Bhaskar, Aardema, Marilyn J., Auerbach, Scott, Boverhof, Darrell, Custer, Laura, Dedon, Peter, Honma, Masamitsu, Ishida, Seiichi, Kasinski, Andrea L., Kim, James H., Manjanatha, Mugimane G., Marlowe, Jennifer, Pfuhler, Stefan, Pogribny, Igor, Slikker, William, Stankowski, Leon F., Tanir, Jennifer Y., Tice, Raymond, van Benthem, Jan, White, Paul, Witt, Kristine L., Thybaud, Véronique, Massachusetts Institute of Technology. Department of Biological Engineering, and Dedon, Peter C.

Subjects
Article
Abstract

Genetic toxicity tests currently used to identify and characterize potential human mutagens and carcinogens rely on measurements of primary DNA damage, gene mutation, and chromosome damage in vitro and in rodents. The International Life Sciences Institute Health and Environmental Sciences Institute (ILSI-HESI) Committee on the Relevance and Follow-up of Positive Results in In Vitro Genetic Toxicity Testing held an April 2012 Workshop in Washington, DC, to consider the impact of new understanding of biology and new technologies on the identification and characterization of genotoxic substances, and to identify new approaches to inform more accurate human risk assessment for genetic and carcinogenic effects. Workshop organizers and speakers were from industry, academe, and government. The Workshop focused on biological effects and technologies that would potentially yield the most useful information for evaluating human risk of genetic damage. Also addressed was the impact that improved understanding of biology and availability of new techniques might have on genetic toxicology practices. Workshop topics included (1) alternative experimental models to improve genetic toxicity testing, (2) Biomarkers of epigenetic changes and their applicability to genetic toxicology, and (3) new technologies and approaches. The ability of these new tests and technologies to be developed into tests to identify and characterize genotoxic agents; to serve as a bridge between in vitro and in vivo rodent, or preferably human, data; or to be used to provide dose response information for quantitative risk assessment was also addressed. A summary of the workshop and links to the scientific presentations are provided., International Life Sciences Institute/Health and Environmental Sciences Institute Committee

Published
2014

150. Histopathological and Molecular Signatures of a Mouse Model of Acute-on-Chronic Alcoholic Liver Injury Demonstrate Concordance With Human Alcoholic Hepatitis.

Author

Furuya, Shinji, Cichocki, Joseph A, Konganti, Kranti, Dreval, Kostiantyn, Uehara, Takeki, Katou, Yuuki, Fukushima, Hisataka, Kono, Hiroshi, Pogribny, Igor P, Argemi, Josepmaria, Bataller, Ramon, and Rusyn, Ivan

Subjects
ALCOHOLIC liver diseases, HIGH cholesterol diet, LIVER, HEPATITIS, HEPATIC fibrosis, ETHANOL, THERAPEUTICS
Abstract

Human alcoholic hepatitis (AH) carries a high mortality rate. AH is an acute-on-chronic form of liver injury characterized by hepatic steatosis, ballooned hepatocytes, neutrophil infiltration, and pericellular fibrosis. We aimed to study the pathogenesis of AH in an animal model which combines chronic hepatic fibrosis with intragastric alcohol administration. Adult male C57BL6/J mice were treated with CCl4 (0.2 ml/kg, 2×weekly by intraperitoneal injections for 6 weeks) to induce chronic liver fibrosis. Then, ethyl alcohol (up to 25 g/kg/day for 3 weeks) was administered continuously to mice via a gastric feeding tube, with or without one-half dose of CCl4. Liver and serum markers and liver transcriptome were evaluated to characterize acute-on-chronic-alcoholic liver disease in our model. CCl4 or alcohol treatment alone induced liver fibrosis or steatohepatitis, respectively, findings that were consistent with expected pathology. Combined treatment resulted in a marked exacerbation of liver injury, as evident by the development of inflammation, steatosis, and pericellular fibrosis, pathological features of human AH. E. coli and Candida were also detected in livers of mice cotreated with CCl4 and alcohol, indicating pathogen translocation from gut to liver, similar to human AH. Importantly, liver transcriptomic changes specific to combined treatment group demonstrated close concordance with pathways perturbed in patients with severe AH. Overall, mice treated with CCl4 and alcohol displayed key molecular and pathological characteristics of human AH—pericellular fibrosis, increased hepatic bacterial load, and dysregulation of the same molecular pathways. This model may be useful for developing therapeutics for AH. [ABSTRACT FROM AUTHOR]

Published
2019
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