Reactive oxygen species (ROS), consisting mainly of superoxide, hydrog
en peroxide and hydroxyl radical, have been implicated in many disease
s including cancer. ROS have been known to play an important role in t
he initiation and promotion of multistage carcinogenesis. The cellular
antioxidant defence plays a crucial role in neoplastic disease. Howev
er, very little is known about the tissue antioxidant defence in thyro
id cancers. We therefore undertook a study to assess the role of ROS i
n the pathogenesis of thyroid cancers, Our samples consisted of post-o
perated thyroid tissues (normal, goiters, follicular adenomas, follicu
lar 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 t
hiols (GSH). Compared to normal thyroid no changes were seen in goiter
s. LP was significantly higher in adenomas (16%) and carcinomas (60-69
%). SOD was decreased by 15% in adenomas while in carcinomas it increa
sed by 9-12%. GPx was raised in carcinomas by 10-21%. Follicular carci
nomas showed a 4% increase in CAT activity while GSH was raised in ade
nomas and papillary carcinomas by 17%. Thus, in adenomas (initial stag
e) involvement of superoxide radicals and in carcinomas (later stage)
hydrogen peroxide and, possibly, hydroxyl radical involvement cannot b
e ruled out. These ROS may be responsible for elevated LP observed in
adenomas and carcinomas.