Elucidating mechanism of drug induced toxicity
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These inhibitors react with their target proteins to form a covalent complex in which the protein has lost its function.The majority of these successful drugs, which include penicillin, omeprazole, clopidogrel, and aspirin were discovered through serendipity in phenotypic screens (Potashman & Duggan, 2009).
Furthermore, there are no specific tools for predicting the occurrence of hepatotoxicity induced by these drugs.
Therefore, there has been considerable interest in elucidating the mechanism(s) of Abeta neurotoxicity.
Here, we review the molecular signaling pathways involved in Abeta-induced cell death, including signaling through the neuronal nicotinic receptor and the Abeta-triggered generation of reactive oxygen species (ROS) leading to the activation of the c-jun N-terminal kinase (JNK), and the ensuing phosphorylation of p66Shc and inactivation of the Forkhead transcription factors.
Methimazole and propylthiouracil have been used in the management of hyperthyroidism for more than half a century.
However, hepatotoxicity is one of the most deleterious side effects associated with these medications.
Genome-wide identification of the mechanism of action (Mo A) of small-molecule compounds characterizing their targets, effectors, and activity modulators represents a highly relevant yet elusive goal, with critical implications for assessment of compound efficacy and toxicity.
Current approaches are labor intensive and mostly limited to elucidating high-affinity binding target proteins.The purpose of this article is to give an overview on possible susceptibility factors in liver injury induced by antithyroid agents.Age, gender, metabolism characteristics, alcohol consumption, underlying diseases, immunologic mechanisms, and drug interactions are involved in enhancing antithyroid drugs-induced hepatic damage. Tel: 98-711-2424-127-238, Fax: 98-711-2424-126, This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.However, with increased understanding of molecular mechanisms, risks for ADRs can be assessed prior to market approval and managed via labeling, education, and/or postmarketing risk evaluation and mitigation strategies established at the time of regulatory approval.The need to collect and store DNA samples in clinical trials to facilitate the identification of genetic basis of ADRs has been emphasized.Covalent bonding thus allows high potency to be routinely achieved in compounds of low molecular mass, along with all the beneficial pharmaceutical properties that are associated with small size (Smith, Zhang, Leach, & Houk, 2009) Covalent inhibitors can be designed to target a nucleophile that is unique or rare across a protein family (Singh et al., 1997)(Cohen et al., 2005)(Singh et al., 2010)(Liu et al., 2013), thereby ensuring that covalent bond formation cannot occur with most other family members.