Time dependent influence of etonogestrel on the caspase-3 immunoreactivity and apoptotic indexes of rat uterus and ovaries

Apoptosis is necessary for the balance between cell proliferation and loss. Thirty-six Wistar-Albino rats were subjected to investigate apoptotic effect of widely used implantable progestins on ovarian and uterine tissues. Rats were divided into 6 groups. In the first five groups, we applied etonogestrel (IMP) subcutaneous implants (n = 30). The rats in groups were sacrificed sequentially every 10 days after application. The rats in the last group (n = 6) were accepted as controls. Apoptotic index (AI) values and Caspase-3 immunoreactivities of ovaries and uterus were recorded. In IMP groups, AI and Hscore values in stroma and glandular epithelium of uterus, granulosa and teca-lutein cells of the ovary increased with the longer progesterone exposure. Increase in AI and Hscore values were more prominent after 30 days of exposure for teca-lutein cells of ovary. Progestins increased apoptosis in ovaries and uterus by the longer exposure. Apoptosis increased in ovaries by chronic progesterone exposure. The apoptotic effect of progestin on endometrium is clear but long-term systemic application may lead to alterations in ovarian physiology. We evaluated time dependent apoptotic effect of etonogestrel on reproductive physiology and discussed progestins effect from another point of view in this study.     

Effects of shock waves on oxidative stress and some trace element levels of rat liver and diaphragm muscles

This study was designed to investigate whether the short-term extracorporeal shockwave lithotripsy (ESWL) exposure to kidney produces an oxidative stress and a change in some trace element levels in liver and diaphragm muscles of rats. Twelve male Wistar albino rats were divided randomly into two groups, each consisting of six rats. The animals in the first group did not receive any treatment and served as control group. The right-side kidneys of animals in group 2 were treated with two-thousand 18 kV shock waves while anesthetized with 50 mg kg(-1) ketamine. The localization of the right kidney was achieved after contrast medium injection through a tail vein under fluoroscopy control. The animals were killed 72 h after the ESWL treatment, and liver and diaphragm muscles were harvested for the determination of tissue oxidative stress and trace element levels. Although the malondialdehyde level increased, superoxide dismutase and glutathione peroxidase enzyme activities decreased in the livers and diaphragm muscles of ESWL-treated rats. Although glutathione level increased in liver, it decreased in diaphragm muscles of ESWL-treated animals. Fe, Mg and Mn levels decreased, and Cu and Pb levels increased in the livers of ESWL-treated animals. Fe and Cu levels increased, and Mg, Pb, Mn and Zn levels decreased in the diaphragm muscles of ESWL-treated animals. It also causes a decrease or increase in many mineral levels in liver and diaphragm muscles, which is an undesirable condition for the normal physiological function of tissues.     

Length–weight relationship of 62 fish species from the Central Aegean Sea,Turkey

Length–weight relationships were estimated for 11 elasmobranch and 51 teleost fish species caught in Izmir Bay, Turkey. Sampling was carried out from June 2005 to May 2006 at monthly intervals using a bottom trawl net. The mean b‐value was calculated as 3.10 (SE = ±0.03) and only three species were out of range between 2.5 and 3.5.     

Effect of Strontium Ranelate on Hydrogen Peroxide-Induced Apoptosis of CRL-11372 Cells

In vitro and in vivo studies have proven strontium to be an osteoinductive trace element. The effect of strontium ranelate (SR) on H₂O₂-induced apoptosis of CRL-11372 cells and optimization of its anti-apoptotic dose were the aims of this study. After 1 h of pretreatment with SR 1 μM, 50 μM, 100 μM, 500 μM, and 1,000 μM concentrations, CRL-11372 osteoblasts were exposed to 100 μM H₂O₂ for periods of 6–12 h. The same experiments were repeated without H₂O₂. The apoptotic index and viability of cells were assessed quantitatively with a fluorescent dye and qualitatively with agarose gel electrophoresis. Concentrations of 1–100 μM of SR with a 6-h treatment and only 1 μM concentration with a 12-h treatment inhibited the apoptotic effect of H₂O₂ on cultured osteoblasts significantly (P < 0.05). SR was shown to inhibit H₂O₂-induced apoptosis of CRL-11372 cells in a dose-dependent manner.     

Evaluation of viscosities of polymer-water solutions used in aqueous two-phase systems

The dynamic viscosities of dilute aqueous poly(ethylene glycol) and dextran, and poly(ethylene glycol)-dextran-water solutions have been measured. The poly(ethylene glycol) and dextran samples had average molecular masses of 8000 Da and 580 000 Da, respectively. To estimate the values of viscosity of poly(ethylene glycol)-dextran-water solutions, a Grunberg like equation has been proposed which takes into account the influence of poly(ethylene glycol) and dextran concentrations. The relative errors vary between 0.76 and 11.64 in absolute value.     

Evaluation of chalcones as inhibitors of glutathione S‐transferase

Glutathione S‐transferases (GSTs) are the superfamily of multifunctional detoxification isoenzymes and play an important role in cellular signaling. In the present study, potential inhibition effects of chalcones were tested against human GST. For this purpose, GST was purified from human erythrocytes with 5.381 EU?mg^?1 specific activity and 51.95% yield using a GSH–agarose affinity chromatographic method. The effects of chalcones on in vitro GST activity were tested at various concentrations. K_i constants of chalcones were found in the range of 7.76–41.93 μM. According to the results, 4‐fluorochalcone showed a better inhibitory effect compared with the other compounds. The inhibition mechanisms of 2'‐hydroxy‐4‐methoxychalcone and 4‐methoxychalcone were noncompetitive, whereas the inhibition mechanisms of 4'‐ hydroxychalcone, 4‐ fluorochalcone, and 4,4'‐ diflurochalcone were competitive.     

Silicon Induced Antioxidative Responses and Expression of BOR2 and Two PIP Family Aquaporin Genes in Barley Grown Under Boron Toxicity

In this study, the effects of boron stress and the application of silicon were investigated on the expression levels of barley homologues of three transporter genes, namely BOR2, PIP1, and PIP1;1, which have potential in transferring boron and silicon into or out of tissues. Boron toxicity in shoot tissues was observed as early as 1-day-long exposure by means of several stress indicators including ion leakage, malondialdehyde (MDA) and H₂O₂ levels. Elemental analysis showed that presence of Si under B stress reduces tissue B levels, whereas B presence increased Si levels in tissues. Presence of silicon induced BOR2 gene expression in shoots during early stress. Presence of both elements simultaneously increased BOR2 expression in both shoot and root tissues, which might be attributed to element similarity. Expression levels of both aquaporin genes PIP1 and PIP1;1 increased in shoots under short term B and Si applications, and levels were more responsive to B when compared to Si. Similar to BOR2 expression, silicon increased both aquaporin gene expressions in shoot tissues under short term boron stress. Investigation of the response of BOR2 and aquaporin genes under boron stress and in the presence of silicon revealed their sensitivity to silicon and their potential function in transporting silicon into tissues. Based on the present work, stress mitigating effects of silicon can be attributed to the competitive role of silicon for the transport via boron transporters under toxic boron levels.

     

Iron metabolism and drug resistance in cancer

Iron is an essential inorganic element for various cellular events. It is directly associated with cell proliferation and growth; therefore, it is expected that iron metabolism is altered in tumor cells which usually have rapid growth rates. The studies on iron metabolism of tumor cells have shown that tumor cells necessitated higher concentrations of iron and the genes of iron uptake proteins were highly over-expressed. However, there are limited number of studies on overall iron metabolism in drug-resistant tumor cells. In this article, we evaluated the studies reporting the relationship between drug resistance and iron metabolism and the utilization of this knowledge for the reversal of drug resistance. Also, the studies on iron-related cell death mechanism, ferroptosis, and its relation to drug resistance were reviewed. We focus on the importance of iron metabolism in drug-resistant cancer cells and how alterations in iron metabolism participate in drug-resistant phenotype.