A5101832177- Alcohol Consumption and Health Effects
- Advanced Glycation End Products research
- Sulfur Compounds in Biology
- Drug-Induced Hepatotoxicity and Protection
- Genomics, phytochemicals, and oxidative stress
- Free Radicals and Antioxidants
- Heavy Metal Exposure and Toxicity
- Phytochemicals and Antioxidant Activities
- Pharmacogenetics and Drug Metabolism
- Metabolism and Genetic Disorders
- Alcoholism and Thiamine Deficiency
- Biochemical effects in animals
- Biochemical Acid Research Studies
- Carcinogens and Genotoxicity Assessment
- Eicosanoids and Hypertension Pharmacology
- Chemotherapy-induced organ toxicity mitigation
- Bioactive Compounds and Antitumor Agents
- Trace Elements in Health
- Folate and B Vitamins Research
- Cancer, Hypoxia, and Metabolism
- Vitamin C and Antioxidants Research
- Toxic Organic Pollutants Impact
- Natural Antidiabetic Agents Studies
- Redox biology and oxidative stress
- Per- and polyfluoroalkyl substances research
University of Toronto
2006-2017
St. Michael's Hospital
2011
Memorial University of Newfoundland
1969-1988
University of Birmingham
1967
Rationale. The toxicity of H2S has been attributed to its ability inhibit cytochrome c oxidase in a similar manner HCN. However, the successful use methemoglobin for treatment HCN poisoning was not poisonings even though ferric heme group scavenges H2S. Thus, we speculated that other mechanisms contribute induced cytotoxicity. Experimental procedure. Hepatocyte isolation and viability enzyme activities were measured as described by , . Results. Incubation isolated hepatocytes with NaHS...
The inactivation of glyceraldehyde-3-phosphate dehydrogenase by hydrogen peroxide has been investigated. reaction obeyed two rate equations: (a) In the absence catalysts (b) presence These Kinetics are identical to those previously observed during glutathione oxidation peroxides. Enzyme was shown be strictly related sulphydryl group modification and this can account for inactivation. For total H2O2, like iodoacetate, modified about 3.5 groups in...
Methotrexate (MTX) is a folic acid antagonist that widely used to treat variety of diseases. One the most serious side effects MTX therapy hepatotoxicity. The potential molecular cytotoxic mechanisms toward isolated rat hepatocytes were investigated using Accelerated Cytotoxicity Mechanism Screening (ACMS) techniques. A concentration and time dependent increase in cytotoxicity reactive oxygen species (ROS) formation decrease mitochondrial membrane (MMP) observed with MTX. Furthermore,...
A large proportion of colorectal cancers are thought to be associated with unhealthy dietary and lifestyle exposures, particularly energy excess, obesity, hyperinsulinemia, hyperglycemia. It has been suggested that these processes stimulate the production toxic reactive carbonyls from sugars such as glyceraldehyde. Glyceraldehyde contributes a group compounds known glyceraldehyde-derived advanced glycation end-products (glycer-AGEs), which may promote cancer through their proinflammatory...
Carbonyls generated by autoxidation of carbohydrates or lipid peroxidation have been implicated in advanced glycation end product (AGE) formation tissues adversely affected diabetes complications. Tissue AGE and associated pathology decreased vitamin B(1)/B(6) trials involving diabetic animal models. To understand the molecular cytoprotective mechanisms involved, effects vitamers against cytotoxicity induced AGE/advanced (ALE) carbonyl precursors (glyoxal/acrolein) compared to oxidative...
Abstract Covalent binding of reactive electrophiles to cellular targets is a molecular interaction that has the potential initiate severe adverse biological effects. Therefore, measure for electrophilic reactivity with nucleophiles could serve as an important correlate toxic effects such hepatocyte death. To determine if electrophile correlates rat cytotoxicity, inherently α , β ‐unsaturated aldehydes were chosen investigation. Reactivity was measured simple assays used glutathione, soft...