Biomedical subjects

Grazyna Bednarek-Tupikowska

Publications and source records attributed to Grazyna Bednarek-Tupikowska.

At least 19 recordsLinked to original sources

PubMed2006

Risk factors of cardiovascular disease in GH-deficient adults with hypopituitarism: a preliminary report.

BACKGROUND: We estimated the influence of GH deficiency (GHD) in adults on chosen risk factors of cardiovascular disease and bone density. MATERIAL/METHODS: Fifty-four adults (mean age: 50.4 years) with hypopituitarism were studied. We measured blood pressure, body mass index, waist-to-hip ratio, total body fat, and bone mineral density and the serum levels of lipids, glucose, insulin, pituitary hormones, estradiol, testosterone, and thyroxine, and the excretion of free cortisol in 24-h urine. GHD was confirmed with the insulin intravenous test (IIT) with a GH response to IIT of <3 microg/ml. The control group consisted of 73 healthy adults. RESULTS: Increased levels of LDL-cholesterol and triglycerides and decreased levels of HDL-cholesterol in the GHD group were observed. Fasting serum glucose and insulin levels were significantly higher in the GHD group than in controls. Significant differences in the QUICKI and FIRI indexes were observed. Twenty-three percent of the hypopituitary patients were hypertensive and 65% were obese. The percentage of total body fat was significantly higher in the studied group than in controls. Thirty-seven percent of the GHD patients were osteoporotic and 23% were osteopenic. CONCLUSIONS: An atherogenic lipid profile, insulin resistance, obesity, and increased body and trunk fat in GHD adults may cause the higher risk of cardiovascular disease in these patients. GHD adults should receive human recombinant GH along with conventional replacement therapy. This may be a useful method in protecting against early onset of atherosclerosis, metabolic disturbances, and osteoporosis, especially in young patients.

Adult↗

PubMed2006

Serum leptin concentrations in pre- and postmenopausal women on sex hormone therapy.

AIM: The aim of the present study was to investigate the influence of endogenous estradiol and estrogen and estrogen-progestin therapies on concentration in pre- and postmenopausal women. MATERIALS AND METHODS: The study groups consisted of 26 women with surgical menopause (mean+/-standard deviation (SD): age 51.8+/-2.6 years, body mass index (BMI) 26.45+/-4.56 kg/m(2)), 54 with natural menopause (mean+/-SD: age 50.5+/-3.0 years, BMI 25.75+/-4.09 kg/m(2)) and 40 premenopausal controls (mean+/-SD: age 48.3+/-2.3 years, BMI 26.23+/-4.12 kg/m(2)). The group with surgical menopause received estradiol transdermally (50 microg/day) and those with natural menopause received additionally medroxyprogesterone acetate (5 mg/day) for the last 12 days of the cycle. Before and after 4 months of therapy, body weight, waist and hip circumferences and blood pressure were measured, and BMI and waist-to-hip ratio (WHR) were calculated. Serum leptin, follicle-stimulating hormone (FSH), estradiol (E(2)), testosterone, prolactin and dehydroepiandrosterone sulfate (DHEAS) were measured prior to and after treatment. RESULTS: Leptin concentrations did not differ statistically among the groups. No correlations between leptin and E(2), FSH, prolactin, testosterone and DHEAS concentrations were found in any of the groups before and after treatment. Leptin level correlated positively with body mass, BMI and hip and waist circumferences in all groups. There were no correlations between leptin and WHR in the pre- and postmenopausal groups. In the premenopausal group and in some postmenopausal groups, serum leptin level correlated with blood pressure. CONCLUSIONS: Endogenous E(2) and androgens in premenopausal women and estrogen and estrogen-progestin therapies in postmenopausal subjects do not influence serum leptin concentrations. Leptin level is related to body mass and BMI, but not to sex hormone status. The distribution of adipose tissue and the type of obesity (android or gynoid) have no influence on serum leptin concentration. The correlation between serum leptin level and blood pressure requires further investigation.

Androgens↗

PubMed2006

Effects of oestradiol and oestroprogestin on erythrocyte antioxidative enzyme system activity in postmenopausal women.

OBJECTIVE: Data concerning the relationship between sex steroid hormones and the cellular antioxidative enzyme system are controversial. We investigated the effects of oestradiol deficiency after menopause and the influence of transdermal oestradiol therapy (ET) and hormonal (oestradiol plus medroxyprogesterone) replacement therapy (HT) on erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT). GSH and selenium (Se) concentrations were also estimated. Serum lipid peroxide (LPO) levels were measured as an indicator of free-radical production and lipid peroxidation. PATIENTS: The study group consisted of 80 postmenopausal women, divided into two subgroups: 26 women with surgically induced menopause (ET1) and 54 women with physiological menopause (HT1). Forty premenopausal healthy volunteers were controls (C group). RESULTS: LPO was higher in postmenopausal women and decreased after both ET and HT. GSH-Px and GSH were lower in the postmenopausal groups but increased significantly after both types of therapy. Se concentrations did not differ significantly among the groups. CAT activities were similar in all groups and decreased after ET and HT. SOD activities in postmenopausal women were similar to those in the C group and did not change significantly after treatment. CONCLUSIONS: The administration of natural oestrogens to postmenopausal women diminishes oxidative stress and increases antioxidative cell potency.

Antioxidants↗

PubMed2006

[Scavenger receptor CD36: its expression, regulation, and role in the pathogenesis of atherosclerosis. Part I].

Atherosclerosis is a progressive pathological process based on endothelial dysfunction and chronic inflammation. Monocytes, macrophages, and modified lipoproteins, especially oxidized LDLs (oxLDLs), play a fundamental role in the pathogenesis of atherosclerosis. Monocytes evolve into macrophages in the vascular wall and then accumulate oxLDLs, forming foam cells. OxLDLs are toxic and activate foam cells, stimulate the replication of macrophages and their migration into atherosclerotic plaque, and increase the expression of metaloproteinases. Macrophages bind oxLDLs through many types of receptors, among them scavenger receptors. One of these is CD36, a membrane glycoprotein expressed by endothelial cells, adipocytes, smooth and skeletal muscle cells, cardiomiocytes, platelets, monocytes, and macrophages. CD36 recognizes and binds many ligands, such as oxLDLs, long-chain fatty acids, collagen, thrombospondin 1, apoptotic cells, anionic phospholipids, and Plasmodium falciparum-infected erythrocytes. CD36 is involved in many processes, e.g. inner immune system responses, removal of apoptotic cells and Plasmodium falciparum-infected erythrocytes, and the transport of long-chain fatty acids, and it also mediates collagen and thrombospondin action. Recent reports indicate that CD36 may play a role in the development of atherosclerosis. An animal model revealed that lack of CD36 expression restrains atheroslerosis. Increased expression of CD36 was shown in atheroslerotic plaque and damaged vascular tissue. Contradictory data about the effects of antiatherosclerotic drugs on CD36 expression indicate the necessity for further investigation of the role of CD36 in the development of atherosclerosis.

Animals↗

PubMed2006

[The influence of diabetes mellitus and insulin resistance on receptor CD36 expression. Part II. The role of receptor CD36 in the pathomechanism of diabetes complications].

Glucose metabolism disorders are significant risk factors for accelerated atherosclerosis, but the exact pathogenesis of this impact and possible co-factors are not precisely known. On the other hand, only two thirds of all atherosclerosis cases are linked to so-called "classic" risk factors, and numerous studies are conducted to recognize those non-classic risk factors, among which homocysteine and adhesive molecules are the most often mentioned. Recently, the class B scavenger receptor CD36 has become an object of interest. Receptor CD36 is a membrane glycoprotein found on the surface of many cells, such as endothelial cells, cardiomyocytes, dendritic cells, platelets, monocytes, and macrophages. Ligands for receptor CD36 are oxidized LDL particles, long-chain fatty acids, collagens, thrombospondin I, apoptotic cells, and phospholipids. Receptor CD36 plays an important role in various processes, e.g. inner immune system response, apoptotic and necrotic cells removal, transport of fatty acids, and inhibition of neoplastic angiogenesis. Scavenging oxidized LDL particles is one of its most important functions. The most recent studies put forward the participation of receptor CD36 in atherogenesis. Additionally, increased CD36 expression has been described in diabetes mellitus and insulin resistance and in the pathogenesis of diabetic macro- and microangiopathy. Confounding data regarding human hereditary receptor CD36 deficiency as well as still unknown interactions between antidiabetic drugs and CD36 expression suggest the necessity for further studies on the participation of receptor CD36 in the atherogenesis linked with glucometabolic disorders and in the development of diabetes mellitus complications.

Animals↗

PubMed2006

[Hypercortisolism in pregnancy].

Hipercortisolemia in pregnancy occurs rarely because of menstrual disturbances and infertility in subjects with Cushing syndrome. The diagnosis of pathological hipercorisolemia in pregnant women is often difficult because some symptoms of the disease may be associated with complicated pregnancy. Hipercortisolemia causes weight gain, especially trunk obesity with thin extremities, arterial hypertension, glucose intolerance, purple-blue skin striae and hirsutism. Hormonal and radiological diagnostic in pregnancy is limited. Results of hormonal estimations and of dynamic tests are difficult to interpret because of physiological changes in the hypothalamo-pituitary-adrenal axis connected with pregnancy. Interpretation of magnetic resonance imaging of pituitary gland should include hypertrophy of pituitary gland connected with pregnancy. The choice of optimal time and method of treatment should be cautious and individualized because of the possibility of maternal and fetal complications.

Adult↗

PubMed2006

A follow-up of 130 patients with acromegaly in a single centre.

OBJECTIVES: Acromegaly is a rare disease with increased mortality rate. The aim was to present our centre experience in the diagnosis and treatment of a series of patients suffering from acromegaly. METHODS: 130 patients (55 men, 75 women) aged 19-84 years presenting with clinical and hormonal features of acromegaly, attending Department of Endocrinology and Out-patient Clinic between 1990 and 2004 were studied. They were analyzed their GH and IGF-1 levels, CT and MRI scans, and they were administered medical therapy, neurosurgery and radiotherapy. RESULTS: We have observed 106 macro-, 16 microadenomas and 1 case of ectopic GHRH. 115 patients were operated, as cured were recognized 74 of them. Pituitary irradiation was applied to 11 patients, in 4 of them it did not cure the disease. Medical therapy was efficacious in 12% patients treated with bromocriptine, 73% with long-acting lanreotide and 58% with long-acting octreotide. In 7 patients other malignant neoplasm were detected. 11 patients died during the follow-up. CONCLUSIONS: There is possible underdiagnosis of acromegaly in our region, especially in males. We have observed better diagnostic opportunities in recent years when MRI was available. It was accompanied by better outcome of surgical and pharmacological treatment and better control of the complications of the disease.

Acromegaly↗

PubMed2005

[Adrenal myelolipoma].

This paper is a review of the literature about adrenal myelolipoma. It is a rare, benign, hormonally inactive tumor of the adrenal gland composed of mature fat tissue and hematopoietic tissue in varying amounts. Adrenal myelolipoma is usually small (< 4 cm), unilateral and causes no clinical disorders. The age range of the affected patients is 20-90 years; most are men in their fourth to sixth decade. This tumour is discovered during autopsy or USG, CT MRI of the abdomen usually by chance and because of that is included in the group of tumors called incidentaloma. Etiology of myelolipoma is unclear. It is usually hormonally inactive but there were several cases in which adrenal myelolipoma coexisted with various endocrine disorders such as Cushing's syndrome, Conn's syndrome, Addison's disease, hirsutism, hermaphroditism, inborn deficiencies of 17- and 21-hydroxylase. It is also more frequent in patients with obesity, hypertension and leading stressful life. Surgical treatment is called for when the diameter of tumor reaches more than 4 cm, tumour shows tendency to fast growth or causes clinical disorders. In cases of small lesions, that show no progression, it is advised to observe the tumor using imaging techniques.

Adrenal Gland Neoplasms↗

PubMed2005

[Non-typical leukemic metastases localization in bulbus oculi and vertebral column and in thyroid gland and trachea in the course of chronic lymphocytic leukemia--two case reports].

Chronic lymphocytic leukemia (CLL) is characterized by the clonal proliferation of small mature lymphocytes with their accumulation in blood, bone marrow, lymph nodes, spleen and lien. In advanced stages of CLL, the leukemic metastases can occur in skin, pleura and lungs. They are often strictly connected with disease progression and are present with advanced lymphadenopathy and hepatosplenomegaly, high leukocytosis 100G/1 with 80-90% lymphocytes in blood smear, anemia Hb <10 g% and thrombocytopenia PLT < 100 G/L. In this article we present two CLL patients with non typical leukemic metastases localization in bulbus oculi, vertebral column (case 1) and in thyroid gland and trachea (case 2), that occurred in hematological stabilization phase of disease during normal lymphocytes number or a little lymphocytosis in peripheral blood and a lack of progression in lymphoid organs.

Aged↗

PubMed2005

[A case of primary hypoparathyroidism and hypothyroidism co-existing with chronic renal failure].

A case of 24-year old woman with chronic renal failure and primary hypoparathyroidism is presented. Primary hypothyroidism and bilateral hypoacousis were also found. Typically concomitant with chronic renal failure is development of secondary hyperparathyroidism and its co-morbidities, i.e. renal osteodystrophy that consists of osteomalacia, osteoporosis and pathological fractures. In case of some patients with very high concentration of parathormone (PTH) and with signs of renal osteodystrophy, which is the case of tertiary hyperparathyroidism, subtotal parathyroidectomy is the optimal treatment. Reduction of PTH concentration protects bones from further destruction and from accumulation of calcium phosphate in tissues. The accompanying primary parathyroid failure would probably protect from the further consequences of PTH over-production--renal osteodystrophy. The case is reported in view of a rare occurrence of such co-existence, lack of its description in Polish literature as well as diagnostic difficulties.

Adult↗

PubMed2005

[The effect of estrogen deficiency, estrogen and estro-progestagene therapy on total plasma homocysteine and serum lipid peroxide levels in postmenopausal women].

OBJECTIVES: Elevated plasma homocysteine (Hcy) concentration is a risk factor for atherosclerosis and venous thrombosis. DESIGN: an observational study. MATERIALS AND METHODS: 120 healthy women were recruited and divided in two subgroups--postmenopausal women (M-80 women) and premenopausal women (40 women) with normal menstruation as control group. 26 women with surgical menopause were treated with percutaneous estrogen therapy and remaining 54 women were treated with estro-progestagen replacement therapy. Measurements of FSH and estradiol was made using radioimmunoassay. HCY was assessed using enzymatic conversion method. RESULTS: Concentrations of Hcy and lipid peroxides (LPO) in postmenopausal study group were higher than in the premenopausal. Treatment with estradiol (E2) alone or in combination with medroxyprogesterone acetate decreased LPO and Hcy concentrations to levels observed in premenopausal group. CONCLUSIONS: Our results suggest that estrogens have a profound influence on Hcy and LPO levels. Reduction in Hcy levels after treatment lowers the production of free radicals and thus contributes to lipid peroxidation decrease and LPO levels reduction after therapy. A practical conclusion may be proposed: in postmenopausal women with elevated Hcy levels who require hormonal replacement therapy, Hcy level control is indicated in order to administer such a therapy, which decreases Hcy concentrations.

Adult↗

PubMed2005

[A long term survival of the patient treated due to advanced adrenocortical carcinoma].

The authors presented a case of 52-years old woman with advanced adrenocortical carcinoma completely recovered after surgical resection followed by chemotherapy and mitotane treatment. Two years later metastatic tumor of hepar was excised. From the first diagnosis - patient lives 12 years, without any symptoms of recurrence until now. The authors accentuate a big value of postoperative control, especially imaging studies for early diagnosis of recurrent of cancer and beginning therapy.

Adrenal Cortex Neoplasms↗

PubMed2005

[Leptin level and the PPARgamma2 Pro12Ala and Pro115Gln polymorphisms in women with functional hyperandrogenism. Preliminary report].

UNLABELLED: Hyperandrogenism is a multifactoral chronic disease, characterised by an androgen excess, often connected with obesity, hirsutism, polycystic ovaries, hyperinsulinemia, insulin resistance and hyperleptynemia. Peroxisome proliferator activated receptors (PPARgamma) are one of the factors influencing insulin sensitivity. As a transcriptional factor it plays a crucial role in the regulation of genes involved in insulin action. The aim of this study was to evaluate the frequency of PPARgamma Pro12Ala and Pro115Gln polymorphisms in hyperandrogenic women. The additional aim was to investigate differences in leptin levels in healthy and FOH (functional ovarian hyperandrogenism) women (non-obese and obese). MATERIAL AND METHODS: we investigated 90 women: 72 healthy women (37 nonobese and 35 obese)--control group, and 18 women with FOH (9 nonobese and 9 obese)--FOH group. We performed anthropological examination: BMI, WHR and total-body densytomery, biochemical and hormonal estimations in the whole group. PPARgamma polymorphism was studied using PCR and RFLP. RESULTS: in the control group Pro12Pro ("wild" type) was observed in 45 women (26 obese and 19 nonobese) - 62.5% of the group. Heterozygosity Pro12Ala was observed in 15 women (20.8%): 4 obese and 11 with BMI < 30 kg/m2, homozygosity Ala12Ala was seen in 12 women (16.6%): 5 obese i 7 nonobese. In FOH group "wild" type was discovered in 9 women (4 obese and 5 nonobese) - 50% of FOH group, heterozygosity Pro12Ala was seen in 5 women (27.7%): 2 obese and 3 with BMI < 30 kg/m2, homozygosityAla12Ala was observed in 4 women (22.2%): 3 obese and in 1 non-obese. Ala allel frequency in control group was 28%. (37% in non-obese and 20% in obese). In FOH group Ala allel frequency was 36% (nonobese - 28%, obese - 44%). In the studied group we did not find Pro115Gln polymorphism. Leptin level in control group was 19.92 +/- 14.3 ng/ml, and in FOH group - 23.41 +/- 19.47 ng/ml. Depending on BMI leptin level in non-obese healthy group was 7.45 +/- 3.76 ng/ml, in non-obese FOH women - 18.33 +/- 16.54 ng/ml, p < 0.005. In obese controls leptin level was 43.6 +/- 17.28 ng/ml, and in obese FOH women - 45.72 +/- 14.89 ng/ml. CONCLUSIONS: Leptin level in non-obese FOH women is significantly higher than in lean healthy controls. This difference was not observed in obese women. However the Pro12Ala polymorphism is quite common; it does not seem to be directly related to the obesity connected with hyperandrogenism. Higher frequency of Ala allele In FOH women compared to healthy controls (36% vs 28%) may at least partially explain the beneficial effect of tiazolidinediones in the treatment of hyperandrogenism.

Adult↗

PubMed2004

[Amiodarone and the thyroid gland].

Amiodarone is an iodine-rich drug. Its chronic administration may lead to disturbances in thyroid hormone metabolism and/or overt gland dysfunction. It causes an increased in serum fT4, rT3, and TSH concentrations and a decreased serum level of fT3 without thyroid dysfunction. Amiodarone may induce thyrotoxicosis (AIT--Amiodarone-induced thyrotoxicosis) or hypothyroidism (AIH--Amiodarone-induced hypothyroidism) in some persons. AIT occurs more frequently in areas with low iodine intake. The excess iodine contributes to excessive thyroid hormone synthesis-type I AIT or may lead to thyroiditis and a destructive process of thyroid follicular cells, resulting in excess thyroid hormone release-type II AIT. The mixed form of AIT also occurs. Type I AIT should be treated with antithyroid drugs alone or in association with potassium perchlorate, type II AIT benefits from treatment with glucocorticoids, whereas the mixed form of AIT is most effectively treated with a combination of thionamides, potassium perchlorate, and glucocorticoids. AIT often requires thyroidectomy after restoration of euthyroidism or radioiodine therapy, provided that 24-h thyroid radioactive iodine uptake values permit. AIH prevails in areas with high dietary iodine intake. It requires a discontinuation of amiodarone therapy and thyroid hormone (levothyroxine) replacement. It can remit spontaneously. Amiodarone and L-thyroxine therapy is also possible. Baseline thyroid function tests, thyroid antibodies, and imaging examinations such as thyroid ultrasound on initial evaluation and follow-ups every 6 months must be carefully monitored before starting amiodarone therapy.

Amiodarone↗

PubMed2004

[Adrenocortical carcinoma and its treatment].

Adrenocortical carcinoma is a rare tumor with an annual incidence of 1 to 2 cases per million people. It is a very aggressive tumor, with a median survival of 28 months, and is slightly more common in women (58.6%) than in men (41.4%). The etiology of disease is still unknown. Most adrenocortical neoplasms are hormone functional. These tumors most commonly produce cortisol (30%), then androgens (20%), estrogens (10%) or aldosterone (2%). The rapid onset of Cushing 's syndrome, with its virilizing features, is characteristic of this cancer. Adrenal tumors are often detected at an advanced stage. In diagnostics, measurement of serum hormone levels and imaging studies, e.g. CT, or MRI, are essential. They also indicate the spread of disease. Complete surgical resection is the only curative treatment for adrenal cancer. Treatment also includes chemotherapy, especially with mitotane, usually in combination with doxorubicin, etoposide, and cisplatin. Results of treatment are not satisfying, so adjuvant multicenter trials are still underway.

Adrenal Cortex Neoplasms↗

PubMed2004

[Homocysteine--an underestimated atheromatosis risk factor. Do sex hormones influence homocysteine concentrations?].

Recent data on the atherogenic effect of elevated concentrations of homocysteine (Hcy) and a review of published results on the influence of sex hormones, especially estrogens, on plasma Hcy levels are presented. Epidemiological data show that hyperhomocysteinemia as well as a mild elevation in plasma Hcy levels significantly increase cardiovascular risk. Some results do not support this relationship. Recently it was established that onset of menopause and decreases in serum estrogen levels probably increase serum Hcy concentrations. The majority of investigation, based on observational studies and the results of one randomized, double-blind placebo-controlled study, showed that use of estrogen and hormonal replacement therapy lowered HCY concentration. It has been observed that the decrease in Hcy level was greater the higher its concentrations before treatment. These results are in contrast with those of another randomized double-blind placebo-controlled study which showed that the Hcy concentration does not depend on menopause and does not change after hormonal treatment. Individual data showed that dehydroepiandrosterone, an adrenal steroid, probably lowers Hcy level. There were no correlations between serum Hcy concentration and insulin concentration, body mass, and type of obesity. The hypotheses about the influence of sex hormones on Hcy concentration are not clear and need further investigation.

Atherosclerosis↗

PubMed2004

[Coexistence of Addison-Biermer's anaemia with endocrine glands' dysfunctions].

Addison-Biermer's anaemia is an autoimmune disease. It may coexist with other auto-aggressive diseases, precede them or join the other existing autoimmune diseases. It most often accompanies the Hashimoto disease but also may coexist polyglandular autoimmune syndrome (PGA). Three types of PGA are distinguished: PGA1--Blizzard's Syndrome, PGA2--Schmidt's Syndrome, and PGA3. The latter, unlike the remaining ones, is characterized by normal function of adrenal glands. Addison-Biermer's anaemia occurrence may be often difficult to diagnose as coexisting illnesses might ouflage its clinical symptoms. The aim of this paper was to analyse patients with different types of PGA with coexisting Addison-Biermer's anaemia. Group of 24 individuals was analysed: 2 women with PGA1, 10 patients with PGA2, 10 patients with PGA3. In 2 remaining ones PGA was not confirmed. Addison-Biermer's anaemia occurred in 7 patients (2 with PGA2 and 5 with PGA3 syndrome). Decreased concentration of vitamin B12 was diagnosed in 3 individuals among 24 examined patients (1 with type 3 and 2 with type 2), as well in 2 patients with unconfirmed PGA. Addison-Biermer's anaemia was not observed in patients with PGA1. We observed that megaloblastic anaemia occurred characteristic schedule depending on appearance of autoimmune diseases: in PGA2--many years after other immunopathies were found, in PGA3--as first auto-aggressive disease. Our analysis suggests the necessity of detailed check-ups on patients with Addison-Biermer's anaemia, as with time they may develop other diseases, especially hypothyroidism and/or PGA failure. On the contrary, in individuals with thyroid gland diseases and PGA syndromes further checkups should be megaloblastic anaemia-sensitive. In both cases it is important to consider substitutive treatment. The possibility of family coexisting both pernicious anaemia and autoimmune endocrinopathies needs diagnostics of members of the patient's family.

Adult↗

PubMed2002

[Antioxidant properties of estrogens].

The author expounded present state of knowledge concerning antioxidant properties of estrogens. Estradiol, apart from its main hormonal effect, probably displays two mechanisms of antioxidant action. One of them results from hydroxyphenolic structure of their molecule. Estradiol may donate hydrogen atoms from its phenolic hydroxyl group to lipid peroxyradicals what results in the termination of the chain reactions of cell membrane phospholipides, which are the key reactions in cell damage. Estradiol also inhibits oxidative modification of LDL lipoprotein which plays the main role in atherogenesis. The other mechanism of antioxidative action of estradiol is probably associated with its stimulatory effect on natural cellular antioxidant enzymes. Data on this subject are scarce and controversial. The mechanisms of antioxidant action of estrogens require further investigation.

Animals↗