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Boric acid as a protector against paclitaxel genotoxicity

100%

Turkez H. , Tatar A. , Hacimuftuoglu A. , Ozdemir E.

Acta Biochimica Polonica

2010

tom 57

nr 1

95-97

Paclitaxel (PAC) is an anticancer drug used for treatments of breast, ovarian and lung cancers. However, little data is; available in the literature on its potential genotoxicity on healthy human cells. On the other hand, boron deficiency and supplementation exert important biological effects in human and animal tissues. The biological effects of dietary boron are defined, but its interaction with PAC is not known for therapeutic uses. The aim of the present study was to determine whether boric acid (BA) confer a protection against PAC genotoxicity. After the application of PAC (10 or 20 μg/l) and BA (2.5 or 5 mg/l), the genotoxic effects were assessed by sister chromatid exchange (SCE) and micronucleus (MN) tests in human blood cultures. We also analyzed nuclear division index (NDI) in peripheral lymphocytes. Our results showed that PAC significantly (P < 0.05) increased the frequencies of SCEs and the formations of MNs in peripheral lymphocytes as compared to controls. PAC decreased the nuclear division index in lymphocyte cultures. Boric acid did not show cytotoxic or genotoxic effects at the concentrations tested. Furthermore, the PAC-induced increases in the genotoxicity and cytotoxicity indices were diminished by the addition of BA. The present study suggests for the first time that BA can prevent the genotoxicity of PAC on human lymphocytes.

Indirect role of beta2-adrenergic receptors in the mechanism of anti-inflammatory action of NSAIDs

88%

Suleyman H. , Halici Z. , Cadirci E. , Hacimuftuoglu A. , Bilen H.

nr 4

661-672

In this study we investigated both intact and adrenalectomized rats to determine whether or not the anti-inflammatory effects of indomethacin, diclofenac sodium, ibuprofen, nimesulide, tenoxicam and aspirin (IDINTA) are related to adrenal gland hormones in carrageenan-induced inflammation model of rats. Also, we investigated the anti-inflammatory action mechanism of hormones (adrenalin, cortisol) which perform a role in the anti-inflammatory effect of IDINTA on the adrenergic receptors. The results show that IDINTA produces significant anti-inflammatory effects in intact rats (ID50: 9.82, 10.81, 95.21, 75.23, 8.21 and 61.84 mg/kg), but insignificant effects in adrenalectomized rats (ID50: 152.97, 188.17, 1275.0, 433.67, 188.16 and 1028.17 mg/kg). In addition, adrenalin and prednisolone caused anti-inflammatory effect rates of 78.3% and 95.7% respectively in adrenalectomized rats. The anti-inflammatory effects of adrenalin and prednisolone did not change when prazosin (1-receptor blocker), yohimbine (2-receptor blocker) and phenoxybenzamine (1- and 2- receptor blocker) were given to rat groups; however, in adrenalectomized rats administered with propranolol (a non-selective blocker of ß1 and ß2-receptors) the anti-inflammatory effect of adrenalin was lost, and that of prednisolone decreased to 36.2%. It was also found that metoprolol (a selective blocker of ß1-receptors) did not alter the anti-inflammatory effects of the drugs. As a result, it was shown that anti-inflammatory effects of IDINTA are related to adrenalin and cortisol (corticosterone in rats). It was also determined for the first time that adrenalin (totally) and prednisolone (partially) triggered anti-inflammatory effects via the ß2-receptors but not via the 1, 2 and ß1-receptors.