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Medical Toxicology Commons

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Full-Text Articles in Medical Toxicology

Suppression Of Peroxisomal Enzyme Activities And Cytochrome P450 4a Isozyme Expression By Congeneric Polybrominated And Polychlorinated Biphenyls, Larry W. Robertson, Isabelle Berberian, Tim Borges, Li-Chuan Chen, Ching K. Chow, Howard P. Glauert, Johannes G. Filser, Helmut Thomas Sep 2007

Suppression Of Peroxisomal Enzyme Activities And Cytochrome P450 4a Isozyme Expression By Congeneric Polybrominated And Polychlorinated Biphenyls, Larry W. Robertson, Isabelle Berberian, Tim Borges, Li-Chuan Chen, Ching K. Chow, Howard P. Glauert, Johannes G. Filser, Helmut Thomas

Toxicology and Cancer Biology Faculty Publications

The purpose of this study was to determine the effects of PCBs and PBBs on peroxisome proliferator-activated receptor-alpha-(PPARalpha-) associated enzyme activities or protein levels. Male Sprague-Dawley rats were administered a single IP injection (150 mu mol/kg) of either 3,3',4,4'-tetrabromobiphenyl, 3,3',4,4'-tetrachlorobiphenyl, 3,3',5,5'-tetrabromobiphenyl, 2',3,3',4,5-pentachlorobiphenyl, 3,3',4,4',5-pentachlorobiphenyl, 2,2',3,3',5,5'-hexachlorobiphenyl, or 3,3',4,4',5,5'-hexabromobiphenyl in corn oil (10 ml/kg). One week later, the activities of catalase, peroxisomal fatty acyl-CoA oxidase, and peroxisomal beta-oxidation as well as cytochrome P450 4A (CYP4A) protein content were determined in subcellular liver fractions. None of the peroxisomal enzyme activities were significantly increased by any of the halogenated biphenyl congeners tested. Except for minor …


High-Dose Pralidoxime For Organophosphorus Poisoning, Ashish Goel, Praveen Aggarwal, Sanjeev Bhoi, Vineet Gupta Apr 2007

High-Dose Pralidoxime For Organophosphorus Poisoning, Ashish Goel, Praveen Aggarwal, Sanjeev Bhoi, Vineet Gupta

Vineet Gupta, MD, FACP

No abstract provided.


Commentary: The Daubert Decision, Robert L. Brent Feb 2007

Commentary: The Daubert Decision, Robert L. Brent

The Selected Works of Robert Brent

No abstract provided.


Comparison Of The Systemic And Pulmonary Inflammatory Response To Endotoxin Of Neutropenic And Non-Neutropenic Rats, Sabrina M. Heidemann, Maria Glibetic Jan 2007

Comparison Of The Systemic And Pulmonary Inflammatory Response To Endotoxin Of Neutropenic And Non-Neutropenic Rats, Sabrina M. Heidemann, Maria Glibetic

Wayne State University Associated BioMed Central Scholarship

Abstract

Background

Neutrophil infiltration commonly occurs in acute lung injury and may be partly responsible for the inflammatory response. However, acute lung injury still occurs in the neutropenic host. The objectives of this study are to determine if inflammation and acute lung injury are worse in neutropenic versus the normal host after endotoxemia.

Methods

Rats were divided into four groups: 1) control, 2) neutropenic, 3) endotoxemic and 4) endotoxemic and neutropenic. Tumor necrosis factor (TNF)-α and macrophage inflammatory protein (MIP-2) were measured in the blood, lung lavage and for mRNA in the lung. Arterial blood gases were measured to determine …


Triumph And/Or Tragedy: The Present Food And Drug Administration Program Of Enriching Grains With Folic Acid., Robert L. Brent Jan 2007

Triumph And/Or Tragedy: The Present Food And Drug Administration Program Of Enriching Grains With Folic Acid., Robert L. Brent

The Selected Works of Robert Brent

No abstract provided.


Developmental Toxicology Drugs, And Fetal Teratogenesis, Robert L. Brent Jan 2007

Developmental Toxicology Drugs, And Fetal Teratogenesis, Robert L. Brent

The Selected Works of Robert Brent

No abstract provided.


How Does The Physician Avoid Prescribong Drugs And Medical Procedures That Have Reproductive And Developmental Risks?, Robert L. Brent Jan 2007

How Does The Physician Avoid Prescribong Drugs And Medical Procedures That Have Reproductive And Developmental Risks?, Robert L. Brent

The Selected Works of Robert Brent

No abstract provided.


Letter To The Editor: Further Efforts To Redce The Incidence Of Neural Tube Defects, Robert L. Brent Jan 2007

Letter To The Editor: Further Efforts To Redce The Incidence Of Neural Tube Defects, Robert L. Brent

The Selected Works of Robert Brent

No abstract provided.


The Folate Debate., Robert L. Brent Jan 2007

The Folate Debate., Robert L. Brent

The Selected Works of Robert Brent

No abstract provided.


Robert Warwick Miller: In Memoriam., Robert L. Brent Jan 2007

Robert Warwick Miller: In Memoriam., Robert L. Brent

The Selected Works of Robert Brent

No abstract provided.


Replication Fork Regression In Vitro By The Werner Syndrome Protein (Wrn): Holliday Junction Formation, The Effect Of Leading Arm Structure And A Potential Role For Wrn Exonuclease Activity, Amrita Machwe, Liren Xiao, Robert G Lloyd, Edward Bolt, David K. Orren Jan 2007

Replication Fork Regression In Vitro By The Werner Syndrome Protein (Wrn): Holliday Junction Formation, The Effect Of Leading Arm Structure And A Potential Role For Wrn Exonuclease Activity, Amrita Machwe, Liren Xiao, Robert G Lloyd, Edward Bolt, David K. Orren

Toxicology and Cancer Biology Faculty Publications

The premature aging and cancer-prone disease Werner syndrome stems from loss of WRN protein function. WRN deficiency causes replication abnormalities, sensitivity to certain genotoxic agents, genomic instability and early replicative senescence in primary fibroblasts. As a RecQ helicase family member, WRN is a DNA-dependent ATPase and unwinding enzyme, but also possesses strand annealing and exonuclease activities. RecQ helicases are postulated to participate in pathways responding to replication blockage, pathways possibly initiated by fork regression. In this study, a series of model replication fork substrates were used to examine the fork regression capability of WRN. Our results demonstrate that WRN catalyzes …


Identification And Characterization Of Ogg1 Mutations In Patients With Alzheimer's Disease, Guogen Mao, Xiaoyu Pan, Beibei Zhu, Yanbin Zhang, Fenghua Yuan, Jian Huang, Mark A. Lovell, Maxwell P. Lee, William R. Markesbery, Guo-Min Li, Liya Gu Jan 2007

Identification And Characterization Of Ogg1 Mutations In Patients With Alzheimer's Disease, Guogen Mao, Xiaoyu Pan, Beibei Zhu, Yanbin Zhang, Fenghua Yuan, Jian Huang, Mark A. Lovell, Maxwell P. Lee, William R. Markesbery, Guo-Min Li, Liya Gu

Toxicology and Cancer Biology Faculty Publications

Patients with Alzheimer's disease (AD) exhibit higher levels of 8-oxo-guanine (8-oxoG) DNA lesions in their brain, suggesting a reduced or defective 8-oxoG repair. To test this hypothesis, this study investigated 14 AD patients and 10 age-matched controls for mutations of the major 8-oxoG removal gene OGG1. Whereas no alterations were detected in any control samples, four AD patients exhibited mutations in OGG1, two carried a common single base (C796) deletion that alters the carboxyl terminal sequence of OGG1, and the other two had nucleotide alterations leading to single amino acid substitutions. In vitro biochemical assays revealed …