Tricyclic Antidepressant Plasma Levels in Overdose

Rudorfer, Matthew V.

doi:10.1001/jama.1981.03310320027012

Cited by 5 publications

(1 citation statement)

References 5 publications

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“…In addition, protein oxidation in the hippocampus 60 and protein carbonyls in the cerebral cortex 58 were significantly elevated in the brains of patients with Alzheimer disease. Claims have been made that Aβ(1–42) 61 , activated microglia 62 , iron accumulation 63 and dysfunctional mitochondria contribute to increased oxidant production 64 .…”

Section: Roles Of Oxidative Stress In Diseasementioning

confidence: 99%

Targeting oxidative stress in disease: promise and limitations of antioxidant therapy

Forman

Zhang

2021

Nat Rev Drug Discov

1,602

818

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Oxidative stress is a component of many diseases, including atherosclerosis, chronic obstructive pulmonary disease, Alzheimer disease and cancer. Although numerous small molecules evaluated as antioxidants have exhibited therapeutic potential in preclinical studies, clinical trial results have been disappointing. A greater understanding of the mechanisms through which antioxidants act and where and when they are effective may provide a rational approach that leads to greater pharmacological success. Here, we review the relationships between oxidative stress, redox signalling and disease, the mechanisms through which oxidative stress can contribute to pathology, how antioxidant defences work, what limits their effectiveness and how antioxidant defences can be increased through physiological signalling, dietary components and potential pharmaceutical intervention.

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Section: Roles Of Oxidative Stress In Diseasementioning

confidence: 99%

Targeting oxidative stress in disease: promise and limitations of antioxidant therapy

Forman

Zhang

2021

Nat Rev Drug Discov

1,602

818

View full text Add to dashboard Cite

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Epigallocatechin-3-gallate improves chronic alcohol-induced cognitive dysfunction in rats by interfering with neuro-inflammatory, cell death and oxido-nitrosative cascade

et al. 2021

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Alcohol consumption for a longer period of time is linked with neuronal damage and an increase in in ammatory signaling resulting in cell death and dementia. Natural compounds are the focus of research due to their high e cacy and good safety pro le. Here we have investigated the effect of chronic epigallocatechin-3-gallate (EGCG) administration against the alcohol-induced cognitive de cit rats. Male Wistar rats were exposed to the ethanol (10 g/kg; oral gavage) for ten weeks and treated with EGCG (25, 50, and 100 mg/kg) for the same duration. Ethanol exposure led to the impaired spatial memory and learning in rats assessed using the Morris water maze and elevated plus-maze test. Further, we assessed the role of EGCG in mitigating the oxidative stress, neuroin ammatory and cell death signaling associated markers. Co-administration with EGCG signi cantly prevented all the behavioral, biochemical and molecular alterations in the different brain regions of ethanol-treated rats in a dose-dependent manner. EGCG suppressed the acetylcholinesterase activity, increased oxidative-nitrosative stress, cytokines (TNF-alpha and IL-1beta), NF-kappa β and caspase-3 levels in both the cortex and hippocampus of ethanol-treated rats. Our preliminary study demonstrated that EGCG improves the oxidonitrosative stress, in ammation, and cell death signaling associated with ethanol-induced cognitive dysfunction. This suggests the potential role of EGCG in mitigating the cognitive de cits associated with chronic alcohol consumption.

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