title: Levothyroxine replacement therapy with vitamin E supplementation prevents oxidative stress and cognitive deficit in experimental hypothyroidism.
abstract: Hypothyroidism has a variety of adverse effects on cognitive function. The treatment of levothyroxine alone cannot restore cognitive defects of hypothyroid patients. Antioxidant vitamin E supplementation could be useful in disturbances which are associated with oxidative stress and could effectively slow the progression of Alzheimer disease. Thus, the purpose of this study was to evaluate oxidative stress status of the serum and hippocampus in hypothyroidism and to examine the effects of levothyroxine replacement therapy with vitamin E supplementation on cognitive deficit. Sprague-Dawley rats were randomly divided into five groups: control group, PTU group, PTU + Vit E group, PTU + L-T4 group, and PTU + L-T4 + Vit E group. Serum and hippocampus malondialdehyde (MDA) levels were determined using the thiobarbituric-acid reactive substances method. Serum and hippocampus superoxide dismutase (SOD) levels were determined by measuring its ability to inhibit the photoreduction of nitroblue tetrazolium. Learning and memory was assessed by Morris water maze test. In the present study, we found that the rats of PTU + Vit E group spent less time to find the platform on days 2, 3, 4, and 5 than the PTU group. Moreover, the rats of PTU + L-T4 + Vit E group spent less time to find the platform on days 4 and 5 than the PTU + L-T4 group. The time spent in the target quadrants was measured in the probe test and no difference was observed in all groups. Oxidative damage has been observed in the serum and hippocampus of hypothyroidism rat. SOD levels of serum and hippocampus tissue were significantly increased and MDA levels were significantly decreased in the PTU + Vit E and PTU + L-T4 + Vit E groups than the PTU and PTU + L-T4 groups. Therefore, these findings indicate that levothyroxine replacement therapy with vitamin E supplementation may ameliorate cognitive deficit in PTU-induced hypothyroidism through the decrease of oxidative stress status.
authors.affiliation: Department of Endocrinology, Anhui Geriatric Institute, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, PR China.
authors.forename: Tianrong
authors.initials: T
authors.lastname: Pan
authors.forename: Mingkui
authors.initials: M
authors.lastname: Zhong
authors.forename: Xing
authors.initials: X
authors.lastname: Zhong
authors.forename: Yanqing
authors.initials: Y
authors.lastname: Zhang
authors.forename: Defa
authors.initials: D
authors.lastname: Zhu
mesh_terms: D000818:Animals; D003072:Cognition Disorders / Q000378:metabolism / Q000517:prevention & control*; D019587:Dietary Supplements; D004195:Disease Models, Animal; D006624:Hippocampus / Q000378:metabolism; D020249:Hormone Replacement Therapy; D007037:Hypothyroidism / Q000139:chemically induced / Q000150:complications* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018782:Maze Learning / Q000187:drug effects / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D011441:Propylthiouracil / Q000009:adverse effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D013974:Thyroxine / Q000494:pharmacology / Q000627:therapeutic use*; D014810:Vitamin E / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D014810:Vitamin E; D008315:Malondialdehyde; D011441:Propylthiouracil; D013482:Superoxide Dismutase; D013974:Thyroxine