ArticleExperimental diabetes research2012
The antioxidant 3H-1,2-dithiole-3-thione potentiates advanced glycation end-product-induced oxidative stress in SH-SY5Y cells.
Article in Experimental diabetes research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Disubstituted Dithiolethione ACDT Exerts Neuroprotective Effects Against 6-Hydroxydopamine-Induced Oxidative Stress in SH-SY5Y Cells.Neurochemical research · 2019Article
- D3T acts as a pro-oxidant in a cell culture model of diabetes-induced peripheral neuropathy.Redox biology · 2019Article
- Effect of Vitis vinifera hydroalcoholic extract against oxaliplatin neurotoxicity: in vitro and in vivo evidence.Scientific reports · 2018Article
- HOxidative medicine and cellular longevity · 2017Article
- Molecular regulatory mechanisms of osteoclastogenesis through cytoprotective enzymes.Redox biology · 2016Review
- New Therapeutic Concept of NAD Redox Balance for Cisplatin Nephrotoxicity.BioMed research international · 2016Review
- Ginseng improves cognitive deficit via the RAGE/NF-κB pathway in advanced glycation end product-induced rats.Journal of ginseng research · 2015Article
- Advanced glycation end products induce oxidative stress and mitochondrial dysfunction in SH-SY5Y cells.In vitro cellular & developmental biology. Animal · 2015Article
- Cisplatin-induced Kidney Dysfunction and Perspectives on Improving Treatment Strategies.Electrolyte & blood pressure : E & BP · 2014Review
- Augmentation of NAD(+) by NQO1 attenuates cisplatin-mediated hearing impairment.Cell death & disease · 2014Article
- Pharmacological activation of NQO1 increases NAD⁺ levels and attenuates cisplatin-mediated acute kidney injury in mice.Kidney international · 2014Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress is implicated as a major factor in the development of diabetes complications and is caused in part by advanced glycation end products (AGEs). AGEs ligate to the receptor for AGEs (RAGE), promoting protein kinase C (PKC)-dependent activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and superoxide radical generation. While scavenging antioxidants are protective against AGEs, it is unknown if induction of endogenous antioxidant defenses has the same effect. In this study, we confirmed that the compound 3H-1,2-dithiole-3-thione (D3T) increases reduced-state glutathione (GSH) concentrations and NADPH:quinone oxidoreductase 1 (NQO1) activity in SH-SY5Y cells and provides protection against H(2)O(2). Surprisingly, D3T potentiated oxidative damage caused by AGEs. In comparison to vehicle controls, D3T caused greater AGE-induced cytotoxicity and depletion of intracellular GSH levels while offering no protection against neurite degeneration or protein carbonylation. D3T potentiated AGE-induced reactive oxygen species (ROS) formation, an effect abrogated by inhibitors of PKC and NADPH oxidase. This study suggests that chemical induction of endogenous antioxidant defenses requires further examination in models of diabetes.
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