Reactive oxygen species (ROS), consisting mainly of superoxide, hydrogen peroxide and hydroxyl radical, have been implicated in many diseases including cancer. ROS have been known to play an important role in the initiation and promotion of multistage carcinogenesis. The cellular antioxidant defence plays a crucial role in neoplastic disease. However, very little is known about the tissue antioxidant defence in thyroid cancers. We therefore undertook a study to assess the role of ROS in the pathogenesis of thyroid cancers. Our samples consisted of post-operated thyroid tissues (normal, goiters, follicular adenomas, follicular carcinomas and papillary carcinomas). The parameters studied were lipid peroxidation (LP), antioxidant enzymes--superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)--and non-protein thiols (GSH). Compared to normal thyroid no changes were seen in goiters. LP was significantly higher in adenomas (16%) and carcinomas (60-69%). SOD was decreased by 15% in adenomas while in carcinomas it increased by 9-12%. GPx was raised in carcinomas by 10-21%. Follicular carcinomas showed a 4% increase in CAT activity while GSH was raised in adenomas and papillary carcinomas by 17%. Thus, in adenomas (initial stage) involvement of superoxide radicals and in carcinomas (later stage) hydrogen peroxide and, possibly, hydroxyl radical involvement cannot be ruled out. These ROS may be responsible for elevated LP observed in adenomas and carcinomas.