Anti-Malondialdehyde polyclonal antibody [Biotin]

Background Radiotherapy is the most common regimen for treating human cancers; however, ionizing radiation (IR) has hazardous effects on metabolically active organs such as the liver. Aim This study aimed to investigate the possible protective (prophylactic and therapeutic) action of taurine against liver damage induced by gamma irradiation at different time intervals as well as the mechanisms by which taurine could provide its potential amelioration actions. Methods In this study, 90 adult male rats (similar to 150 g) were randomly divided into five groups. Group 1 is the control group, group 2 received an oral daily dose (500 mg/kg) of taurine for two weeks, group 3 was exposed to a whole-body single dose of gamma-irradiation (6 Gy), and groups 4 and 5 received taurine before or after gamma-irradiation, respectively. Six rats from each group were sacrificed after 1, 2, and 3 weeks. Results Over the period of the 3 weeks studied, there were significant increases in MDA, NO, TNF-alpha, and cytochrome-c levels and ALT, caspases-9 and -3 activities and significant decreases in GSH, SOD, CAT, and GPx in the irradiated group when compared with the relevant control. The liver of irradiated rats showed dilatation in the central and portal veins, edema, and degenerated hepatocytes. Conclusions Taken together, IR caused maximum devastation in the liver 2 weeks after exposure as shown by elevation of the inflammatory and apoptotic markers and reducing the antioxidants. Taurine was able to alleviate the deleterious biochemical and histological effects whether given before or after IR. The magnitude of the observed protective effects was in both cases very similar.

Mononuclear and binuclear Ru-II/arene/triphenylphosphine complexes with p-substituted benzoic acid derivatives were prepared and characterized. These monocationic complexes of type [Ru(eta(6)-p-cymene)(PPh3)L] (L = benzoic acid (1), p-hydroxybenzoic acid (2), p-nitrobenzoic acid (3) and terephthalic acid (4)) were characterized using various techniques, such as nuclear magnetic resonance (NMR) and matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry, and the crystal structure of 1, 3 and 4 were determined by X-ray diffraction analysis. The cytotoxicity of the complexes was evaluated, in vitro, against tumorigenic [MDA-MB-231, MCF-7 (breast), A549 (lung) and DU-145 (prostate)] and non-tumorigenic [MCF-10A (breast), MRC-5 (lung) and PNT-2 (prostate)] cells. The binuclear complex (4) was inactive due to its low solubility. Complexes 1, 2 and 3 showed similar cytotoxicity, however, complex 1 presented better selectivity index against MDA-MB-231 than compounds 2 and 3. Cellular ruthenium absorption was explored by inductively coupled plasma mass spectrometry (ICP-MS) analyzing the whole cells and the culture medium. Complementary studies showed that complex 1 inhibited colony formation, induced morphology changes in cells and promoted cell cycle arrest in the Sub-G1 phase for the MDA-MB-231 cells.