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 groups: a control, a
superoxide dismutase (SOD 8 x 10(4) IU/L), and a
catalase group (1 x 10(6) IU/L), and three groups treated with h-
thioredoxin [approximately .01 microM (TRX-I group), approximately 0.1 microM (TRX-II group), and approximately 1 microM (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 approximately 0.1 micro was the most effective.