ORIGINAL ARTICLE Hypothyroidism alters antioxidant defence system in rat brainstem during postnatal development and adulthood Srikanta Jena • Shravani Bhanja Received: 21 October 2013 / Accepted: 20 February 2014 Ó Springer-Verlag Italia 2014 Abstract The present investigation was carried out to evaluate alterations in oxidative stress parameter [lipid peroxidation (LPx)] and antioxidant enzyme activities [superoxide dismutase (SOD), catalase (CAT) and gluta- thione peroxidase (GPx)] in rat brainstem in response to neonatal hypothyroidism during development (from birth to 7, 15 and 30 days old) and adulthood (90 days old). Hypothyroidism in rats was induced by feeding the lac- tating mothers (from the day of parturition till weaning, 25 days old) or directly to the pups with 0.05 % [6-n- propyl 2-thiouracil (PTU)] in drinking water. Increased level of LPx was observed in brainstem of 7 days old hypothyroid rats, accompanied by augmented activities of SOD and GPx. In 15 and 30 days old hypothyroid rat brainstem, a significant decline in LPx was observed. Significantly increased activities of CAT and GPx were observed in 15 and 30 days PTU-treated rats. Decreased level of LPx was observed in brainstem of rats treated with PTU from birth to 30 days followed by withdrawal up to 90 days of age (transient hypothyroidism) as compared to control and persistent treatment of PTU up to 90 days of age. Activities of CAT and GPx were decreased in per- sistent hypothyroid rats of 90 days old with respect to control and transient hypothyroid rats. On the other hand, SOD activity was decreased in both persistent and transient hypothyroid rats with respect to control rats. These results suggest that the PTU-induced neonatal hypothyroidism modulates the antioxidant defence system during postnatal development and adulthood in brainstem of rats. Keywords Neonatal hypothyroidism  Brainstem  Antioxidant enzymes  Oxidative stress Introduction Thyroid hormones have been unequivocally shown to play a key role in brain development. Several studies report in detail the significance of thyroid hormones (TH) in the developing brain, especially the cerebrum and cerebellum [1–4]. One of the important functions of thyroid hormones is to determine the cellular basal metabolic rate, oxygen consumption as well as active oxygen metabolism [5–7]. Numerous authors have shown that altered thyroid states modulate the production of cellular reactive oxygen species (ROS) in adult rats [8–10]. Many studies including ours report that altered thyroid states provoke alterations in antioxidant defence system in various tissues including several brain regions [11–16]. However, similar studies reporting the role of TH deficiency on active oxygen metabolism in the brainstem are scanty [17]. The brainstem is known to play a vital role in the reg- ulation of consciousness, sleep–wake cycle, respiratory and cardiovascular control [18]. It is also the key centre that provides transit between nuclei of the ascending and descending pathways between cerebrum, cerebellum, and spinal cord as well as integrates actions of the sensory fibers terminating in brainstem nuclei and motoneurons originating in brainstem nuclei. The brainstem consists of several nerve fibres apart from brainstem nuclei and is enriched with polyunsaturated fatty acids making it vul- nerable to attack by ROS. Reactive oxygen species are byproducts of normal metabolism in all aerobic cells. Of the oxygen consumed by cells, most of it is tetravalently reduced to water during mitochondrial respiration, S. Jena (&)  S. Bhanja Department of Biotechnology, Utkal University, Bhubaneswar 751004, Odisha, India e-mail: jenasrikanta@yahoo.co.in 123 Neurol Sci DOI 10.1007/s10072-014-1697-5