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排序方式: 共有72条查询结果,搜索用时 15 毫秒
1.
The protective effect of arbutin against potassium bromate-induced oxidative damage in the rat brain
H. Turan Akkoyun Ahmet Uyar Mahire Bayramoglu Akkoyun Aydın Şükrü Bengü Şule Melek Fatma Karagözoğlu Sevinç Aydın Suat Ekin Sinem Aslan Erdem 《Journal of biochemical and molecular toxicology》2023,37(2):e23248
This study aimed to investigate the protective effects of arbutin (ARB) against brain injury induced in rats with potassium bromate (KBrO3). The rats were divided into four groups as Group 1: Control (0.9% NaCl ml/kg/day p.), Group 2: KBrO3 (100 mg/kg (gavage), Group 3: ARB (50 mg/kg/day p.), and Group 4: KBrO3 + ARB (100 mg/kg (gavage) + 50 mg/kg/day p.). At the end of the fifth day of the study, the rats in all groups were killed, and their brain tissues were collected. In the collected brain tissues, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels were measured, and routine histopathological examinations were made. The MDA levels in the group that was exposed to KBrO3 were significantly higher than those in the control group (p ˂ 0.001). In comparison to the KBrO3 group, the MDA levels in the KBrO3 + ARB group were significantly lower (p ˂ 0.001). It was observed that SOD and CAT enzyme activity levels were significantly lower in the KBrO3 group compared to the control group (p ˂ 0.001), while these levels were significantly higher in the KBrO3 + ARB group than in the KBrO3 group (p ˂ 0.001). Additionally, the group that was subjected to KBrO3 toxicity, as well as ARB administration, had much lower levels of histopathologic signs than the group that was subjected to KBrO3 toxicity only. Consequently, it was found that KBrO3 exposure led to injury in the brain tissues of the rats, and using ARB was effective in preventing this injury. 相似文献
2.
Paul G. Braunschweiger Vathsala S. Basrur Dayna Cameron Laura Sharpe Octavio Santos James P. Perras Bernd-Uwe Sevin Arnold M. Markoe 《Biotherapy》1997,10(2):129-137
The modulation of cisPlatin cytotoxicity by interleukin-1 (IL-1α) was studied in cultures of SCC-7 tumor cells with and without
tumor macrophages to examine potential mechanisms for the synergistic antitumor activity of cisPlatin and IL-1α in SCC-7 solid
tumors. Neither IL-1α nor tumor macrophages affected the survival of clonogenic tumor cells and IL-1α had no direct effect
on tumor cell growthin vitro. Macrophages had no direct effect on cisPlatin sensitivity (IC90=6.0 μM), but, the addition of IL-1α (500–2000U/ml) to co-cultures of cisPlatin pretreated tumor cells and resident tumor
macrophages increased cell killing (IC90=3.1 μM). Similar responses were seen in primary cultures treated with cisPlatin before IL-1α. The modulation of cisPlatin
cytotoxicity by IL-1α exhibited a biphasic dose response that paralleled the IL-1α dose dependent release of H2O2by resident tumor macrophages. Further, IL-1α modification of cisPlatin cytotoxicity was prompt and inhibited by catalase.
CisPlatin and exogenous H2O2 (50 μM) produced more than additive SCC-7 clonogenic cell kill and hydroxyl radicals played an important role in the response.
Interleukin-1 modulation of cisPlatin cytotoxicity was schedule dependent. IL-1α treatment for 24 hrs, before cisPlatin, produced
drug resistance (IC90=11.1 μM). Our study shows that IL-1α can stimulate tumor macrophages to release pro-oxidants that modify cellular chemosensitivity
in a schedule and dose dependent fashion. Our findings may also provide a mechanistic explanation for the synergistic antitumor
activity of cisPlatin and IL-1αin vivo. 相似文献
3.
4.
Kai Hilpert Dirk FH Winkler Robert EW Hancock 《Biotechnology & genetic engineering reviews》2013,29(1):31-106
Spatial organization of metabolic enzymes may represent a general cellular mechanism to regulate metabolic flux. One recent example of this type of cellular phenomenon is the purinosome, a newly discovered multi-enzyme metabolic assembly that includes all of the enzymes within the de novo purine biosynthetic pathway. Our understanding of the components and regulation of purinosomes has significantly grown in recent years. This paper reviews the purine de novo biosynthesis pathway and its regulation, and presents the evidence supporting the purinosome assembly and disassembly processes under the control of G-protein-coupled receptor (GPCR) signaling. This paper also discusses the implications of purinosome and GPCR regulation in drug discovery. 相似文献
5.
A key requirement for encoding the auditory environment is the ability to dynamically alter cochlear sensitivity. However,
merely attaining a steady state of maximal sensitivity is not a viable solution since the sensory cells and ganglion cells
of the cochlea are prone to damage following exposure to loud sound. Most often, such damage is via initial metabolic insult
that can lead to cellular death. Thus, establishing the highest sensitivity must be balanced with protection against cellular
metabolic damage that can lead to loss of hair cells and ganglion cells, resulting in loss of frequency representation. While
feedback mechanisms are known to exist in the cochlea that alter sensitivity, they respond only after stimulus encoding, allowing
potentially damaging sounds to impact the inner ear at times coincident with increased sensitivity. Thus, questions remain
concerning the endogenous signaling systems involved in dynamic modulation of cochlear sensitivity and protection against
metabolic stress. Understanding endogenous signaling systems involved in cochlear protection may lead to new strategies and
therapies for prevention of cochlear damage and consequent hearing loss. We have recently discovered a novel cochlear signaling
system that is molecularly equivalent to the classic hypothalamic–pituitary–adrenal (HPA) axis. This cochlear HPA-equivalent
system functions to balance auditory sensitivity and susceptibility to noise-induced hearing loss, and also protects against
cellular metabolic insults resulting from exposures to ototoxic drugs. We review the anatomy, physiology, and cellular signaling
of this system, and compare it to similar signaling in other organs/tissues of the body. 相似文献
6.
7.
Novel anti-infectives: is host defence the answer? 总被引:2,自引:0,他引:2
8.
Burcu Erbaykent Tepedelen Mehmet Korkmaz Ertugrul Tatlisumak Elgin Türköz Uluer Ercüment Ölmez İsmail Değerli Elif Soya Sevinç İnan 《Biological trace element research》2017,178(2):210-217
Evidences about the preventive and therapeutic effects of boron compounds on cancer have been increasing in the last years. Although calcium fructoborate (CaFB) is used as a nutritional supplement, data about its preventive and therapeutic effects on neoplastic transformations are limited. In the present study, the various concentrations of CaFB were applied to the MDA-MB-231 metastatic breast cancer cell line. First, we examined the cytotoxic effect and IC50 value of CaFB by MTT assay. For the evaluation of the DNA damage, apoptosis and metastatic potential, expression levels of ATM, pATM, PARP, p53, p-p53, caspase-3, caspase-9, and VEGF were investigated by using immunoblotting and immunohistochemical methods. Cell viability was significantly reduced at 50 μM CaFB treatment. pATM, p-p53, and caspase-9 levels increased significantly in all groups; furthermore, there was approximately 12.5-, 2.4-, and 10.7-fold increase, respectively, for 100 μM CaFB treatment. ATM and p53 levels did not change with CaFB treatment, but PARP levels significantly 2.5-fold decreased. While VEGF immunoreactivity decreased in all groups, significant increase in caspase-3 immunoreactivity was observed only in the group treated with 50 μM CaFB (p < 0,001). Our results imply that CaFB may have therapeutic potential as well as preventive benefits in cancer. 相似文献
9.