brain tissues oxidative damage as a possible mechanism of deleterious effects of propylthiouracil- induced hypothyroidism on learning and memory in neonatal and juvenile growth in rats

introduction: the role of brain tissues oxidative damage in learning and memory impairments has been well documented. it is also well known that thyroid hormones have a critical role for the brain functions. the purpose of this study was to investigate the role of brain tissues oxidative damage as a possible mechanism of deleterious effects of propylthiouracil (ptu) - induced hypothyroidism on learning and memory in neonatal and juvenile growth in rats. methods: fourteen pregnant female wistar rats were kept in separate cages. after delivery, they were randomly divided into two groups including control and ptu. rats in the control group received normal drinking water, whereas the second group received drinking water supplemented with 0.02% ptu from the first day after delivery through the first two months of the life of offspring (the pups of rats). after 60 days, nine male offspring of each group were randomly selected and tested in the morris water maze (mwm). then, samples of blood were collected to measure thyroxine. finally, the brains were removed and total thiol groups and molondialdehyde (mda) concentrations were determined. results: compared to the control group’s offspring, serum thyroxine levels in the ptu group’s off spring were significantly low (p<0.001). in mwm, the escape latency and traveled path in the ptu group were significantly higher than that in the control group (p<0.01- p<0.001). in ptu group, the total thiol concentrations in both cortical and hippocampal tissues were significantly lower and mda concentrations were higher than control group (p<0.001). discussion: it seems that deleterious effect of hypothyroidism during neonatal and juvenile growth on learning and memory is at least in part due to brain tissues oxidative damage.