Volume 37, Issue 3

Background Although numerous studies have proven that estrogen (Est) has a protective effect on the development of hypertension, more research needs to be done to show its detailed mechanism in a variety of hypertension. The important role of active oxygen species in blood pressure is well defined. We examined whether or not sex hormones change the growth of reactive oxygen species (ROS) ‎in kidneys after central microinjection of angiotensin II (Ang II).‎ Materials and methods Female Wistar rats, 8 weeks old (200 ± 10 g) were used in this study. The animal groups were (1) Sham, (2) Ovariectomy (OVX), (3) Sham-Hypertension (Sham-Hyper), (4) OVX-Hypertension (OVX-Hyper), (5) Sham-Hyper-Est, (6) OVX-Hyper-Est‎;‎ (7) Sham-Hyper-Testosterone (Tst) and (8) OVX-Hyper-Tst. Solutions of 1% NaCl and 0.1 KCl ‎were used and desoxycorticostrone (doca-salt) was injected (45 mg/kg) 3 times a week in Hypertension groups. Estradiol and Tst (2 mg/kg and ‎5 mg/kg‎; daily; subcutaneously) for 4 weeks. Ang II (50 μM, 5 μL) was microinjected by intracerebroventricular ( i.c.v.) infusion and malondialdehyde (MDA) and thiol in the kidneys were measured. Results MDA in the kidneys was increased by Ang II and doca-salt treatments. Both estradiol and Tst decreased the kidney’s MDA. The level of thiol was higher in Hyper ‎groups and reversed after treatment with estradiol and Tst. Conclusions Our findings suggest that central effect of Ang II on blood pressure and kidney ‎disease is accompanied with increased levels of oxidative stress in the kidneys. Indeed sex hormones change the ROS level in the kidneys after central ‎microinjection of Ang II.‎‎

Background Resistin and retinol-binding protein 4 (RBP4) can work in an intricate in metabolic syndrome (MetS) and prediabetes (PreDM) molecular crosstalk. Materials and methods Resistin and RBP4 were evaluated using colorimetric enzyme-linked immunosorbent assays (ELISAs) in 29 normoglycemic MetS, 30 newly diagnosed drug naïve MetS-preDM patients and 29 lean and normoglycemic controls. Results In this cross-sectional design; the gradual increase in resistin levels (ng/mL), though not ascribed any statistically marked variation, was appreciable in both normoglycemic and preDM MetS groups vs. controls. RBP4 mean circulating levels (ng/mL) in both MetS groups (non-diabetic and preDM) invariably lacked discrepancy vs. controls. Except for fasting plasma glucose (FPG) and A 1C ; no further intergroup discrepancy could be identified between MetS arms. Adiposity indices: body mass index (BMI), body adiposity index (BAI) and lipid accumulation product (LAP) (but not conicity index) were substantially higher in both MetS (non- and preDM) groups vs. those of controls. Likewise, the atherogenicity index of plasma [but not non-high-density lipoprotein-cholesterol (nonHDL-C)/HDL-C ratio, or triglyceride (TG)/HDL-C ratio] or any of the hematological indices [red cell distribution width (RDW-CV %), monocyte to lymphocyte ratio (MLR), neutrophil to lymphocyte ratio (NLR) and platelet (PLT) to lymphocyte ratios (PLR)] had any marked variations as compared to controls. Low-density lipoprotein-cholesterol (LDL-C)/HDL-C ratio,visceral adiposity index, and waist circumference (WC)/hip circumference (HC) ratio were noticeably greater in MetS-preDM vs. normoglycemic MetS recruits. Neither biomarker could relate to each other, or any of the atherogenecity indices in 59 MetS participants (non- and preDM). Unlike RBP4; resistin associated proportionally with each of HC, BAI, MLR and NLR. Conclusions Both biomarkers can be putative indicator/surrogate prognostic tools for the prediction/prevention and pharmacotherapy of MetS anomalies.

Background Ghrelin and zinc finger BED domain-containing protein 3 (ZBED3) are distinctively cross linked with prediabetes (preDM) and metabolic syndrome (MetS). Materials and methods In a cross-sectional design with 29 normoglycemic MetS and 30 newly diagnosed drug naïve preDM/MetS patients vs. 29 lean and normoglycemic controls; ghrelin and ZBED3 were evaluated using colorimetric enzymatic assays. Results While ZBED3 mean circulating levels (ng/mL) in both MetS groups (normoglycemic and preDM) invariably lacked discrepancy vs. controls; Appreciably ghrelin levels (ng/mL) in preDM/MetS (but not normoglycemic MetS) participants were markedly higher vs. controls. Except for fasting plasma glucose (FPG) and glycosylated-hemoglobin (HbA 1C ); no further intergroup discrepancy could be identified between the MetS arms. Remarkably adiposity indices (body mass index (BMI), body adiposity index (BAI), and lipid accumulation product (LAP), but not conicity index (CI) or visceral adiposity index (VAI)); atherogenicity index of plasma (but not non-high-density lipoprotein-cholesterol (non-HDL-C/HDL-C) ratio, or total cholesterol (TC)/HDL-C ratio) or any of hematological indices (red cell distribution width (RDW-CV%), monocyte to lymphocyte ratio (MLR), neutrophil to lymphocyte ratio (NLR) and platelet (PLT) to lymphocyte ratio (PLR)) were substantially higher in both MetS (non- and preDM) groups vs. those of controls. Exceptionally low-density lipoprotein -cholesterol (LDL-C)/HDL-C ratio, and waist circumference (WC)/hip circumference (HC) ratio were much more pronounced in MetS-preDM vs. normoglycemic MetS recruits. In the MetS pool (both normoglycemic and preDM, n = 58), neither biomarker could relate to each other, or any of clinical parameters, adiposity or atherogenecity indices. Exceptionally ghrelin correlated significantly and inversely with age. ZBED3 correlated significantly and directly with RDW-CV% in the same pool of MetS recruits (n = 59). Conclusions Both biomarkers can not be ruled out as putative predictive/surrogate prognostic tools for metabolic anomalies prevention and pharmacotherapy.

Background The main aim of this study was to assess the serum levels of copper (Cu), zinc (Zn) with lipid peroxidation, Cu/Zn superoxide dismutase (Cu/Zn SOD) activity, and ceruloplasmin (Cp) in multiple myeloma (MM) patients. Materials and methods The study was conducted in 34 MM patients at stage I. Serum Cu and Zn levels were measured by atomic absorption spectrometry. Also, spectrophotometric assays of malondialdehyde (MDA) levels in addition to Cp and Cu/Zn SOD were quantitated. Results The results showed a significant decrease in the serum Zn levels in patients with MM (p < 0.0001). Also, serum Cu levels were significantly higher (p < 0.0001). However, the serum Cu/Zn ratio was significantly higher in the cancer patients (p < 0.0001). A significant difference was observed in the patients group compared with the control group according to the Cu/Zn SOD activity (p < 0.0001). Moreover, serum levels of Cp and MDA were significantly increased in patients (p < 0.0001, both). Conclusions The elevated levels of serum Cu and MDA with a decrease in Zn and Cu/Zn SOD might explain the increased oxidative stress in MM disease. As the high Cu level was observed in MM patients, therefore, Cu levels should be concentrated in the pathogenesis and progression of MM disease.

Background The objective was to estimate ovarian reserve in adolescent girls born prematurely. Materials and methods Two hundred adolescent girls aged 15–16 years who were born prematurely and full term were studied with laboratory, ultrasound and statistical methods. Results Statistically significant differences of the main parameters that characterize ovarian reserve in adolescent girls born prematurely compared to those born full term were specified. The levels of estradiol (p = 0.027), anti-Müllerian hormone (p = 0.0004) and inhibin В (p = 0.015) were lower in the girls born prematurely and follicle stimulating (p = 0.0001) and lutenizing (p = 0.002) hormone levels were higher. The ultrasound imaging (USI) findings of the uterus and appendages were also different. Adolescent girls born prematurely had longer uterus cervix, smaller sizes of endometrial echo, smaller ovarian sizes and fewer follicles in them. Conclusions Adolescent girls born prematurely have different parameters of ovarian reserve compared to those of girls born full term.