The study was aimed at demonstrating changes in the antioxidant defense systems [Reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT)] forming an antioxidative barrier and oxidative stress parameter (Malondialdehyde = MDA) in the various tissues of Sprague-Dawley rats which were administrated plant growth regulators (PGRs) [Abcisic acid (ABA) and Gibberellic acid (GA(3))] during 25 days. Seventy five parts per million of ABA and GA(3) as drinking water were administered orally to rats (Sprague-Dawley albino) ad libitum for 25 days continuously. The PGRs treatments caused different effects on antioxidant defense systems and MDA content of experimented rats compared to controls. The lipid peroxidation end product MDA significantly increased in the spleen and lungs of rats treated with ABA and GA(3) without significantly change in the other tissues. The GSH levels were significantly increased in the lungs and stomach of rats treated with ABA without any change in the tissues of rats treated with GA(3). Antioxidant enzyme activities such as SOD significantly increased in the spleen of rats treated with ABA and GA(3). Meanwhile, SOD significantly increased in the kidney of rats treated with GA. CAT significantly decreased in the lungs treated with ABA but did not change significantly in all the rest of rat tissues treated with both the PGRs. On the other hand, the ancillary enzyme GR activity decreased in the spleen and increased in the kidney with GA(3) treatment. The drug metabolizing enzyme GST activity significantly decreased in the heart of rats treated with GA(3) but increased in the spleen and lungs of rats treated with both PGRs. The observations presented led us to conclude that administration of subacute ABA and GA(3) promotes lipid peroxidatin content and alters in the antioxidative systems in the rat's various tissues. These data, along with changes, suggest that the PGRs produced oxidative stress in rats during the period of a 25-day subchronic exposure. (C) 2007 Elsevier B.V. All rights reserved.