Biomedical subjects

Ewa Sewerynek

Publications and source records attributed to Ewa Sewerynek.

8 recordsLinked to original sources

PubMed2006

Effect of propylthiouracil on the level of Schiff's bases in tissues of rats on diet with different doses of potassium iodide.

OBJECTIVES: Iodide administration to animals, living in iodine-deficient areas, can induce oxidative processes in the thyroid gland and increase concentration of lipid peroxidation (LPO). Propylthiouracil (PTU)--a well-known antithyroid drug--may also act as an antioxidant. There are some reports, which consider the protective ability of this drug against LPO. The goal of the study was to evaluate oxidative processes and the protective role of PTU in three rat organs during treatment with pharmacological doses of iodide. MATERIAL AND METHODS: Schiff's bases (SB) concentrations (a parameter of oxidative stress) were measured in liver, lung and kidney homogenates of male Wistar rats. For 2 weeks the animals received iodides in their diet in the following concentrations: Group 1--Controls (standard diet, approx. 0.7 mg of potassium iodide per kg; KI/kg); Group 2--diet containing 0.25 mg KI/kg; Group 3--diet with 4.0 mg KI/kg; Group 4--diet with 8.0 mg KI/kg. Group 5--standard diet with 0.1% of PTU in drinking water for two weeks. Subsequent tree groups (6-8) received KI in their diet in doses as above, respectively, together with PTU. RESULTS: We noted increased SB levels in the lungs and in the liver, compared to those observed in the control group. We also found decreased SB concentrations in liver and lung homogenates after the administration of PTU but, unexpectedly, the level of SB increased in kidney homogenates of all the groups. CONCLUSIONS: The results of this study indicate that iodine is involved in oxidative processes in different organs and PTU protects against iodine-induced oxidative stress.

Animals↗

PubMed2006

Potassium iodide changes the levels of thyroid hormones in goitrogenic rats on selenium deficient diet.

OBJECTIVE: A possible link was proposed between selenium [Se(-)], iodine deficiency and thyroid pathology. The aim of the study was to examine changes in FT3 and FT4 concentrations, weights of the thyroid glands and ioduria after potassium iodide (KI) in normal and goitrogenic rats on Se(-) diet. METHODS: Wistar rats in Group 1 received the standard diet. Other animals remained (3 months) either on a Se(-) diet alone [Groups 2-5] or supplemented with selenium [Se(+)] (Group 6-8). After 9 weeks, Groups 3, 4, 6, 7 received sodium perchlorate [I(-); 1 month]. KI (1 mg/rat) was injected in Groups 4, 5, 7, 8. The animals were decapitated 3 days after the injections. RESULTS: FT4 was higher in serum of Se(-) rats than in that of Se(+). The differences of FT3 were not statistically significant. In I(-) Groups, the levels of FT3 and FT4 were very low. KI increased both thyroid hormones in I(-) rats but the effect was especially pronounced for FT3. KI decreased the weights of the glands, enlarged in the I(-) animals, both on Se(-) and Se(+) diet. Urine iodide concentrations were lower in Se(-) animals; KI increased ioduria. CONCLUSIONS: These data demonstrate that selenium and iodine deficiencies may play an essential role in thyroid hormone metabolism.

Animals↗

PubMed2005

Effects of different antioxidants on lipid peroxidation in brain homogenates, induced by L-thyroxine administration in rats.

OBJECTIVE: It is known that thyrotoxicosis induces lipid peroxidation (LPO). In contrast, propylthiouracil (PTU), a thyrostatic drug is a well-known antioxidant. Also melatonin has been shown to protect against free radical-induced neuronal destruction. At the same time, it is generally accepted that the brain is the most vulnerable tissue to oxidative stress. METHODS: The goal of the study was to examine the components of LPO, i.e., conjugated dienes (CD), malondialdehyde (MDA) and Schiff's bases (SB), in the brain of male Wistar rats. Two experiments were performed, with two control groups created for each experiment: Group 1--intact animals and Group 2--animals injected with 0.9% NaCl. In Experiment I, the animals received L-thyroxine (L-T4) in a dose of 100 microg/kg BW, i.p., daily, for two weeks (Groups 3-5). After one week of L-T4 treatment, the following agents were added during a subsequent week: Group 4--PTU in drinking water (45 mg/kg BW/day); Group 5--melatonin (5 mg/kg BW, daily). In Experiment II, lasting 7 days, the animals were divided into the following groups: Group 1--intact animals; Group 2--animals injected with 0.9% NaCl; Group 3--PTU in drinking water (45 mg/kg BW/day); Group 4--melatonin (5 mg/kg BW, daily). RESULTS: In Experiment I, we observed a significantly higher SB level in saline treated animals and a significant increase in both CD and SB levels in rats treated with L-T4, compared to those in non treated control. CD levels were also elevated in rats treated with L-T4, compared to values in the saline only treated animals. Melatonin and PTU reduced CD levels and melatonin diminished SB levels, as compared to those in L-T4-treated rats. In Experiment II, we observed significantly higher CD, SB and MDA levels in saline treated rats, when compared to respective values in non treated control. Melatonin decreased CD levels, when compared to CD levels in both the non treated and saline injected controls. Additionally, melatonin reduced SB levels relative to change in the brains of saline treated rats. Furthermore, PTU decreased CD levels in brain homogenates compared to non-treated animals. CONCLUSIONS: (1) L-thyroxine administration stimulates LPO in the rat brain; (2) All the examined antioxidants decrease LPO in L-T4-administered animals; (3) All the examined antioxidants reduce the basal LPO; 4) Stress, when induced by handling, intensifies oxidative processes in the organism.

Analysis of Variance↗

PubMed2002

Melatonin and the cardiovascular system.

Melatonin concentrations in serum, as well as urinary levels of its main metabolite, 6-sulphatoxymelatonin, decrease with age. In the course of aging, the frequency of heart diseases, both acute and chronic, systematically increases. The evidence from the last 10 years suggests that melatonin influences the cardiovascular system. The presence of vascular melatoninergic receptors/binding sites has been demonstrated; these receptors are functionally linked with vasoconstrictor or vasodilatory effects of melatonin. Melatonin can contribute in cardioprotection of the rat heart, following myocardial ischemia. It has been shown that patients with coronary heart disease have a low melatonin production rate, especially those with higher risk of cardiac infarction and/or sudden death. There are clinical data reporting some alterations of melatonin in human stroke and coronary heart disease. The suprachiasmatic nucleus and, possibly, the melatoninergic system may also modulate cardiovascular rhythmicity. Hypercholesterolemia and hypertension are the other age-related symptoms. People with high levels of LDL-cholesterol have low levels of melatonin. It has been shown that melatonin suppresses the formation of cholesterol by 38% and reduces LDL accumulation by 42%. A 10-20% reduction of cholesterol concentration in women using the B-oval pill has been observed. It is a very important because, even a 10-15% reduction in blood cholesterol concentration has bee shown to result in a 20 to 30% decrease in the risk of coronary heart disease. People with hypertension have lower melatonin levels than those with normal blood pressure. The administration of the hormone in question declines blood pressure to normal range. It has been observed that melatonin, even in a dose 1 mg, reduced blood pressure and decreased catecholamine level after 90 min in human subjects. Melatonin may reduce blood pressure via the following mechanisms: 1) by a direct effect on the hypothalamus; 2) as an antioxidant which lowers blood pressure; 3) by decreasing the level of catecholamines, or 4) by relaxing the smooth muscle in the aorta wall.

Animals↗

PubMed2000

Thymidine kinase and adenosine kinase activities in homogenates of thyroid lobes in hemithyroidectomized rats; effects of melatonin in vitro.

OBJECTIVES: Thymidine kinase (TK, EC 2.7.1.21) is a part of the pyrimidine salvage pathway, involved in DNA synthesis. In turn, adenosine kinase (AK, EC 2.7.1.20) functions as a part of the purine metabolic pathway, involved in DNA synthesis. Melatonin (Mel) is an indoleamine which is known to inhibit growth processes in the thyroid gland and also in other endocrine and non-endocrine tissues. The aim of our study was to examine TK and AK activities in homogenates of the rat thyroid lobes remaining after contralateral hemithyroidectomy (hemiTx); additionally, incubations with Mel (10(-6), 10(-9), and 10(-12) M) were performed. METHODS: The experiment was performed on young male Wistar rats (6-week old). The enzyme activities were measured by ascending chromatography and expressed as the amounts of radioactive reaction products of the phosphorylation of dThd (for TK) and of dAdo (for AK). RESULTS: 1. HemiTx increased TK activity in homogenates of the remaining thyroid lobe; 2. Mel increased TK activity in all the groups (intact, sham-operated- and hemiTx-rats), except for the concentrations of 10(-9) and 10(-12) M in the hemiTx-rats, in which the increasing effects of Mel on TK activity reached the borderline statistical significance only; 3. Mel increased the AK activity in intact and in shamTx animals; 4. No statistically significant changes were found in AK activity following Mel in vitro in the incubated remaining thyroid lobes, collected from hemiTx-rats.

Journal Article↗

PubMed1999

Effects of melatonin on the oxidative stress induced by thyrotoxicosis in rats.

High concentrations of thyroid hormones can affect the metabolism of oxygen in aerobic conditions and stimulate free radicals generation in mitochondria. Reactive oxygen species are toxic to biomembranes and lead to peroxidation of lipids unless they are not removed by free radical scavengers. A few years ago melatonin (MEL), a pineal hormone, was described as a scavenger of free radicals, especially of hydroxyl and peroxyl radicals. The goal of the study was to examine the parameters of oxidative stress [the levels of conjugated dienes (CD), malondialdehyde (MDA) and Schiff bases (SB)] in male rats with thyrotoxicosis, induced by the injection of L-thyroxine (L-T4) in a dose of 100 &mgr;g/kg B.W. After one week of treatment with L-T4, the animals received MEL in a dose 5 mg/kg B.W., i.p., daily, for 7 days. Diagnosis of thyrotoxicosis was confirmed, using hormonal assays. We observed the increased concentration of free T4 (fT4) and free T3 (fT3) after L-T4 injections. The concentration of fT3 was diminished after MEL in L-T4-injected animals. In the liver, we did not observe any changes in the content of both CD and MDA after L-T4 injections but the content of SB was higher after L-T4 injections when compared to the control group. In the liver, melatonin did not change any parameters of oxidative stress, either alone or after L-T4. The changes in the parameters of oxidative stress were better expressed in the kidney, compared to the liver. Melatonin decreased the concentration of CD and SB in the kidneys of a group of animals with thyrotoxicosis. Additionally, MEL decreased the basal concentrations of CD and SB, when compared to the control group.

Journal Article↗

PubMedDate not supplied

Melatonin effects on Schiff's base levels induced by iodide administration in rats.

OBJECTIVES: Administration of iodides to animals, living in iodine-deficient areas, can induce necrosis and fibrosis of the thyroid gland. It is believed that structural and functional changes of the thyroid may be related to oxidative processes. Increased lipid peroxidation levels were reported in murine thyroid glands after high doses of iodine. Melatonin (MEL) is believed to exert its effects via electron donation to directly detoxify free radicals, such as, e.g., the highly toxic hydroxyl radical. In numerous reports related to the antioxidative action of MEL, the authors have considered the protective ability of this hormone against peroxidation of lipids. The goal of the study was to evaluate oxidative processes and the protective role of MEL in three organs of the rat (the liver, the brain, and the lungs) during treatment with different doses of iodide. MATERIAL AND METHODS: Schiff's bases (SB) concentrations (a parameter of oxidative stress) were measured in liver, lung and brain homogenates of male Wistar rats. The animals received iodides in their diet in the following concentrations, for 2 weeks: Group 1--Controls (standard normal-iodine diet, containing approx. 0.7 mg of kalium iodide per kg; KI/kg); Group 2--diet containing 0,25 mg KI/kg; Group 3--diet with 4,0 mg KI/kg; Group 4--diet with 8,0 mg KI/kg. Group 5--standard normal-iodine diet and MEL alone in a dose of 1 mg/kg BW i.p. at 3.00 pm, every day for two weeks. Subsequent three groups (6-8) received KI in their diet in doses as above, respectively, together with MEL. RESULTS: We noted increased levels of SB in the lungs and in the liver, when compared to those observed in controls. We also found decreased SB concentrations in liver and lung homogenates after an administration of MEL but--unexpectedly--the level of SB increased in the group with the highest dose of iodine in diet in lung homogenates. Increased levels of Schiff's bases suggest that iodine is involved in oxidative processes not only in the thyroid but also in other tissues, and MEL protects against the iodine-induced oxidative stress. CONCLUSION: Our results confirm the differences in lipid peroxidation among the examined organs. These alterations can possibly be related to different sensitivity rates of examined tissues to oxidative damage.

Animal Feed↗

PubMedDate not supplied

Evaluation of bone mineral density on the basis of the results of studies of selected skeleton populations from the microregion of Brześć Kujawski.

INTRODUCTION: Osteoporosis is a systemic disease of the skeletal system characterised by reduced bone strength leading to increased risk of fracture. Bone strength is a combined derivative of bone mineral density (BMD) and of bone tissue quality. Osteoporosis is a serious medical problem because of its complications, most frequently manifesting itself in spine fractures, fractures of distal sections of the forearm and, in later periods of life, hip fractures. Reduced BMD is an independent risk factor of osteoporosis. The goal of the study was an evaluation of bone mineral density of the population inhabiting the micro-region of Brześć Kujawski from the 11(th) century until the beginning of the 19th century. MATERIAL AND METHODS: Human bones obtained from archaeological excavations at four archaeological sites: Kolonia (11th-13th centuries), SBK-4 (12th-16th centuries), Fara (14th-17th centuries) and Swiety Duch (16th-19th centuries) and from the collections of the Katedra of Anthropology of the University of Łódź were subjected to study. Bone mineral densities of the skeleton populations were compared with those of the control group, namely the present living population of the Łódź Province. The incidence of osteoporosis was evaluated by densitometric assessment, which was performed by dual energy X-ray absorptiometry (DXA) on a DPX device (LUNAR, USA). RESULTS: The densitometric measurements performed enabled differences to be identified in the mineral density of the osseous tissue. The skeletal groups studied were characterised by a significantly higher mean BMD than the contemporary living population. Changes in BMD indicative of osteopenia prevailed in women. CONCLUSIONS: On the basis of the results obtained it cannot definitively be stated that the skeletal groups studied, despite their significantly higher BMD, were affected by a lower risk of osteoporosis and its complications. A continuation of studies on the mineral content of bones and on the relationship between the mineral content and bone mineral density is required.

Absorptiometry, Photon↗