title: Pinealectomy increases oxidant damage in kidney and testis caused by hyperthyroidism in rats.
abstract: Thyroid hormones regulate energy metabolism and act on mitochondria which are an important source of free radicals in the cell. The pineal gland activates antioxidant systems via melatonin secretion and thus has a protective function in body tissues. The present study was conducted to determine the oxidative damage caused by hyperthyroidism in kidney and testis tissues of pinealectomized rats. Experimental animals were allocated to three groups: 1, control group; 2, sham pinealectomy-hyperthyroidic group; and 3, pinealectomy-hyperthyroidic group. Hyperthyroidism was induced by A 3-week intraperitoneal administration of thyroxin after sham pinealectomy or pinealectomy. Malondialdehyde (MDA) and glutathione (GSH) levels were determined in kidney and testis tissues. MDA levels of the kidney and testis tissue in the pinealectomy and hyperthyroidic groups were significantly higher than those in the sham pinealectomy-hyperthyroidic group and the control group (p < 0.001). GSH levels of both kidney and testis tissues were significantly higher in the sham-pinealectomy-hyperthyroidic group when compared to the other two groups (p < 0.001). This increase in GSH levels was more evident in the pinealectomy-hyperthyroidic group than in the control group (p < 0.001). The results of our study demonstrate that MDA and GSH levels in kidney and testis tissues increased due to hyperthyroidism and that pinealectomy made the increase in MDA levels more apparent, while decreasing GSH levels.
authors.affiliation: Department of Physiology, Meram Medical School, Selcuk University, Konya, Turkey. mogulkoc@selcuk.edu.tr
authors.forename: Rasim
authors.initials: R
authors.lastname: Mogulkoc
authors.forename: Abdulkerim Kasim
authors.initials: AK
authors.lastname: Baltaci
authors.forename: Leyla
authors.initials: L
authors.lastname: Aydin
authors.forename: Esma
authors.initials: E
authors.lastname: Oztekin
authors.forename: Isik
authors.initials: I
authors.lastname: Tuncer
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004734:Energy Metabolism; D005978:Glutathione / Q000378:metabolism; D006980:Hyperthyroidism / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D016877:Oxidants / Q000378:metabolism; D018384:Oxidative Stress; D010870:Pineal Gland / Q000378:metabolism* / Q000601:surgery*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013737:Testis / Q000378:metabolism* / Q000473:pathology
chemical_list: D016877:Oxidants; D008315:Malondialdehyde; D005978:Glutathione