The effect of lithium tetraborate as a novel cardioprotective agent after renal ischemia-reperfusion injury

Abstract Epidemiological studies suggest that acute kidney injury has certain effect on myocardial function. In this study, for the first time, we tested a boron compound namely lithium tetraborate an act as an anti-oxidant and anti-inflammatory agent in ischemia-reperfusion injury. For this, we employed an in vivo rat model with kidney ischemia reperfusion injury to evaluate cardiac injury to clarify the mechanisms of lithium tetraborate. The evaluation of cardiac injury through kidney artery occlusion and reperfusion rat model indicated that lithium tetraborate could (1) reduce oxidative stress-induced endothelial dysfunction; (2) attenuate the inflammatory response of cardiac cells; and (3) alleviate the apoptosis and necrosis of myocytes. In summary, lithium tetraborate demonstrates significant therapeutic properties that contribute to the amelioration of cardiac damage, and it could be a promising candidate for future applications in myocardial dysfunction.

Extract of the Punica granatum Flowers Attenuates Progression of Hepatoxicity against Cadmium Chloride-Induced Liver Injury in Rats

Background: In the present study, we investigated the role of cadmium in acute liver injury, as well as the underlying mechanisms. Methods: On the other hand, we investigated whether Punica granatum flower extract (PG) has a healing effect on CD-induced liver damage. Control groups (G1-G2) received water and 200 mg/kg PG, respectively. Toxicity groups (G3-G6) received 2 different doses of Cd (15-30 mg/kg b.w) orally in a single administration. To evaluate liver function, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and γ-glutamyl transferase (GGT) were detected in the serum, superoxide dismutase (SOD), glutathione peroxidase (GPx), thiobarbituric acid reactive substances (TBARS) were established in the liver and 8-hydroxy-20-deoxyguanosine (8-OHdG) levels were determined for the antioxidative and anti inflammatory effects of PG. Tissue sections were also evaluated histopathologically. Results: We found that Cd exposure decreased levels of SOD, GPx and, increased expression of caspase-3 and levels of TBARS and 8-OHdG. Biochemical and histopathological analysis revealed the toxic effects of cadmium on the liver for the rats in oral acute toxicity study. Functional parameters were significantly improved in PG-treated groups and the severity of the liver injury and apoptosis were significantly decreased in this group. Conclusion: As a result, PG can be consumed as a protective agent against acute liver injuries.

Protective effect of sodium selenite against the genotoxicity of aflatoxin B1 in human whole blood cultures

This study was designed to investigate the effects of selenium and aflatoxin on human whole blood cultures (WBC) in relation to induction of sister-chromatid exchange (SCE). The results showed that the frequency of SCEs in peripheral lymphocytes was significantly increased by the direct-acting mutagen AFB1 (at doses 5 and 10 µM except for 1µM) compared to controls. When sodium selenite (Na2SeO3) was added alone at a molar ratio of 5x10-7 and 1x10-6, cells did not show significant increase in SCE frequency. Whereas, SCE rates induced by the various AFB1 concentrations could be significantly reduced by the presence of Na2SeO3 in a clear dose-related manner. These results indicated that selenite and AFB1 mutually antagonized their ability to cause DNA damage leading to the formation of SCEs. However, selenium didn't completely inhibit induction of SCEs by AFB1 compared to controls. This is first report describing, the protective ability of selenium againist AFB1 genotoxicity on human WBC.

Protective effect of sodium selenite on genotoxicity to human whole blood cultures induced by aflatoxin B1

The aim of this study was to investigate the effects of selenium and aflatoxin on human whole blood cultures (WBC) in relation to induction of sister-chromatid exchange (SCE). Results showed that the frequency of SCEs in peripheral lymphocytes was significantly increased by the direct-acting mutagen AFB1 (at doses 5 and 10 æM except for 1æM) compared with controls. When sodium selenite (Na2SeO3) was added at a molar ratio of 5x10-7 and 1x10-6, cells did not show significant increase in SCE frequency. Whereas, SCE rates induced by the various AFB1 concentrations could be significantly reduced by the presence of Na2SeO3 in a clear dose-related manner. These results indicated that selenite and AFB1 mutually antagonized their ability to cause DNA damage leading to the formation of SCEs. However, selenium didn't completely inhibit induction of SCEs by AFB1 compared with controls. AFB1 induced oxidative damage contributed to its genotoxicity in human WBC.