Protection Against Reperfusion-Induced Arrhythmias by Human Thioredoxin

• Published in: Journal of cardiovascular pharmacology Vol. 27; no. 5; pp. 727 - 732
• Main Authors: Aota, Masaki, Matsuda, Katsuhiko, Isowa, Noritaka, Wada, Hiromi, Yodoi, Junji, Ban, Toshihiko
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA Lippincott-Raven Publishers 01-05-1996; Hagerstown, MD Lippincott
• Subjects: Animals; Arrhythmias, Cardiac - prevention & control; Biological and medical sciences; Cardiovascular system; Catalase - pharmacology; Humans; Male; Medical sciences; Miscellaneous; Myocardial Reperfusion Injury - prevention & control; Pharmacology. Drug treatments; Rats; Rats, Wistar; Recombinant Proteins - pharmacology; Superoxide Dismutase - pharmacology; Thioredoxins - pharmacology; Heart; Adult T cell leukemia; Rat; Arrhythmia; Cardiovascular disease; Superoxide dismutase; Thioredoxin; Reperfusion; Catalase; Ischemia; Heart disease; Lymphoproliferative syndrome; Cell factor; Enzyme; Rodentia; Retroviridae; Malignant hemopathy; In vitro; Infection; Virus; Vertebrata; Mammalia; Peroxidases; Viral disease; Analog; Animal; Oxidoreductases; HTLV-I virus
• ISSN: 0160-2446; 1533-4023
• DOI: 10.1097/00005344-199605000-00016

Adult T-cell leukemia-derived factor (ADF), identified in the supernatant of adult T-cell leukemia (ATL) cell culture, is a human homologue of thioredoxin and consists of 104 amino acids; it has two redox-active half-cysteine residues in an exposed active center. Human thioredoxin has many biological activities, including growth promotion, cell activation, and a catalase-like radical scavenging activity. We examined the protective effect of human thioredoxin (h-thioredoxin) against reperfusion-induced arrhythmias in an isolated rat heart model with 10-min regional ischemia followed by 30-min reperfusion. Male Wistar rats were assigned to six groupsa control, a superoxide dismutase (SOD 8 × 10 IU/L), and a catalase group (1 × 10 IU/L), and three groups treated with h-thioredoxin [≈0.01 μM (TRX-I group), ≈0.1 μM (TRX-II group), and ≈1 μM (TRX-III group)]. In the early reperfusion period, h-thioredoxin reduced the incidence of ventricular fibrillation (VF) to 8% in the TRX-II group (p < 0.01) from the control value of 75%. SOD and catalase reduced the incidence of VF to 43 and 33%, respectively (NS). During the entire reperfusion period, the incidence of VF in the SOD group was 79%, as compared to 83% in the control group. In the catalase and TRX-II groups, the incidence of VF was significantly reduced to 42 and 25%, respectively. These findings indicate that SOD failed to protect against the reperfusion-induced arrhythmias. h-Thioredoxin exerted a protective effect against these arrhythmias; a concentration of ≈0.1 μM was the most effective.