Cardiovascular complications of Khat.

This article reviews current knowledge in khat (cathinone) research and its health impacts and toxicity in the cardiac system of khat chewers based on current evidence. The authors describe the process by which khat is postulated to induce multiple cardiac abnormalities by illustrating multiple case reports as described from around the world. The role of free radicals in inducing cardiac disease is also discussed.

Khat a drug of abuse: roles of free radicals and antioxidants.

Many articles have reviewed the health impact of Khat consumption; however the role of free radicals in the pathogenesis associated with short- and long-term consumption of Khat is absent in the literature. As free radicals and antioxidants converge across various mechanisms in normal physiological function and in disease, this review attempts to uncover the role of endogenous free radicals and the mechanism of cellular injury associated with Khat consumption.

Free radicals are present in human serum of Catha edulis Forsk (Khat) abusers.

Objective: Khat (Catha edulis Forsk) is a naturally occurring drug with an amphetamine-like structure and action. It has been postulated that amphetamine induces free radical formation. On this basis, we have hypothesized that Khat may promote synthesis of reactive oxygen and nitrogen species in the same way that amphetamine promotes free radical production.

Cardiac blood biomarkers in patients receiving thoracic (chemo)radiation.

Cardiotoxicity is a known consequence of thoracic irradiation and there are multiple overlapping risk factors for cardiac disease and thoracic malignancies. In this study, we quantified the impact of thoracic (chemo)radiation on cardiac troponin T (TnT), creatine kinase-myocardial band (CK-MB) and aminoterminal pro-brain natriuretic peptide (NT-proBNP). Thirty patients receiving radiation therapy to the thorax with or without concurrent chemotherapy were evaluated.

Fatty acid methyl esters are detectable in the plasma and their presence correlates with liver dysfunction.

Background: Methanol is a component of certain alcoholic beverages and is also an endogenously formed product. On this basis, we have proposed that methanol may promote synthesis of fatty acid methyl esters (FAMEs) in the same way that ethanol promotes fatty acid ethyl ester (FAEE) synthesis. We tested the hypothesis that FAMEs appear in the blood after ethanol intake.