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Inhibition of renal NQO1 activity by dicoumarol suppresses nitroreduction of aristolochic acid I and attenuates its nephrotoxicity.
  • Min Chen, L. Gong, +9 authors Jin Ren
  • Biology, Medicine
  • Toxicological sciences : an official journal of…
  • 1 August 2011
Aristolochic acid I (AAI) is the major toxic component of aristolochic acid that causes aristolochic acid nephropathy and Balkan endemic nephropathy. Nitroreduction is an essential metabolic processExpand
Knockout of hepatic P450 reductase aggravates triptolide-induced toxicity.
Triptolide, the primary active component of Tripterygium wilfordii Hook F, has various pharmacological activities but also a narrow therapeutic window. Cytochrome P450s are proposed to be responsibleExpand
Critical role of organic anion transporters 1 and 3 in kidney accumulation and toxicity of aristolochic acid I.
Ingestion of aristolochic acid (AA), especially its major constituent aristolochic acid I (AAI), results in severe kidney injury known as aristolochic acid nephropathy (AAN). Although hepaticExpand
Metabolism, Genotoxicity, annd Carcinogenicity of Comfrey
Comfrey has been consumed by humans as a vegetable and a tea and used as an herbal medicine for more than 2000 years. Comfrey, however, produces hepatotoxicity in livestock and humans andExpand
Hepatic cytochrome P450s play a major role in monocrotaline-induced renal toxicity in mice
Aim:Monocrotaline (MCT) in plants of the genus Crotalaria induces significant toxicity in multiple organs including the liver, lung and kidney. Metabolic activation of MCT is required for MCT-inducedExpand
1H NMR-based metabolomic analysis of triptolide-induced toxicity in liver-specific cytochrome P450 reductase knockout mice
Triptolide (TL) is an active component of Tripterygium wilfordii Hook. F which is used to treat autoimmune and inflammatory disease. However, a high incidence of adverse effects is often observed inExpand
Potassium bromate treatment predominantly causes large deletions, but not GC>TA transversion in human cells.
Potassium bromate (KBrO(3)) is strongly carcinogenic in rodents and mutagenic in bacteria and mammalian cells in vitro. The proposed genotoxic mechanism for KBrO(3) is oxidative DNA damage. KBrO(3)Expand
Emodin triggers DNA double-strand breaks by stabilizing topoisomerase II-DNA cleavage complexes and by inhibiting ATP hydrolysis of topoisomerase II.
  • Y. Li, Yang Luan, +9 authors Jin Ren
  • Biology, Medicine
  • Toxicological sciences : an official journal of…
  • 1 December 2010
Emodin, an anthraquinone derived from a plant and fungi, has been reported to possess potential genotoxicity, but the mechanism is not entirely clear. Here, we report that emodin causes DNAExpand
Targeting the MYCN–PARP–DNA Damage Response Pathway in Neuroendocrine Prostate Cancer
Purpose: We investigated MYCN-regulated molecular pathways in castration-resistant prostate cancer (CRPC) classified by morphologic criteria as adenocarcinoma or neuroendocrine to extend theExpand
Genotoxic effects of imidacloprid in human lymphoblastoid TK6 cells
Abstract Among neonicotinoid insecticides, the fastest growing class of insecticides worldwide over the past decade, imidacloprid (IMI) is the most widely used one. The effects of IMI on humanExpand
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