Effect of dietary boron on learning and behavior in rats administered with boric acid.

This study was designed to investigate the effect of dietary boron on spatial learning, anxiety, some vitamins and oxidative parameters in rats. Thirty-two Wistar albino male rats were used in the study. The rats were equally divided into four groups with 8 rats each: I control group: standard pellet diet only, II. group: 250 ppm boric acid, III. group: 500 ppm boric acid and IV. group: 1000 ppm boric acid added into standard pellet diet. Over a five-week period, elevated plus-maze test was used for anxiety assessment and Morris water maze test was used for evaluating spatial learning. Additionally, blood samples were obtained at the end of the experiment and were used to determine the serum levels of some vitamins and oxidative parameters. Dietary boron significantly increased weight gain (p<0.001) and food consumption in the 250 ppm and 500 ppm groups (p<0.05). Although boron supplementation had no significant effect on learning and anxiety-related behavior, it had beneficiary effects on memory retention in the 1000 ppm group (p<0.05). Biochemical analyses showed a significant decrease in the MDA levels (p<0.05) and an increase in vitamin D3 levels (p<0.01) in the 500 ppm group, a significant increase in GSH-Px activity in the 250 ppm and 500 ppm groups (p<0.05), and a decrease in vitamin E levels in all the experimental groups (p<0.05). In conclusion, our study demonstrated that dietary boron can be beneficial for health when administered at appropriate doses.

Cardiac glycoside-induced cell death and Rho/Rho kinase pathway: Implication of different regulation in cancer cell lines.

Previously, we demonstrated that the Rho/ROCK pathway is involved in ouabain-induced apoptosis in HUVEC. In the current work, we investigated whether the Rho/ROCK pathway is functional during cardiac glycosides-induced cytotoxic effects in cancer cell lines, as well as in non-tumor cells. For that purpose, we evaluated the role of ROCK activation in bleb formation and cell migration over upstream and downstream effectors in addition to ROCK cleavage after cardiac glycosides treatment. All three cardiac glycosides (ouabain, digoxin and bufalin) induced cell death in HeLa and HepG2 cells and increased the formation of blebbing in HeLa cells. In contrast to our previous study, ROCK inhibitor Y27632 did not prevent bleb formation. Observation of ROCK II cleavage after ouabain, digoxin and oxaliplatin treatments in HeLa and/or HepG2 cells suggested that cleavage is independent of cell type and cell death induction. While inhibiting cleavage of ROCK II by the caspase inhibitors z-VAD-fmk, z-VDVAD-fmk and z-DEVD-fmk, evaluation of caspase 2 siRNA ineffectiveness on this truncation indicated that caspase-dependent ROCK II cleavage is differentially regulated in cancer cell lines. In HeLa cells, ouabain induced the activation of ROCK, although it did not induce phosphorylation of ERM, an upstream effector. While Y27632 inhibited the migration of HeLa cells, 10nM ouabain had no effect on cell migration. In conclusion, these findings indicate that the Rho/ROCK pathway is regulated differently in cancer cell lines compared to normal cells during cardiac glycosides-induced cell death.