MATERIALS AND METHODS: The antioxidant effect of these compounds was initially performed in vitro using 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2,2-azinobis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assay methods before subjecting them to in vivo experiments. Compounds showing potent antioxidant activity (CS-1 and CS-2) were investigated further for their antidepressant activity using the forced swim test (FST) and tail suspension test (TST). Ascorbic acid (AA) and fluoxetine (20 mg/kg, p.o) were used as reference drugs for comparison in the antioxidant and antidepressant experiments, respectively.
RESULTS: It was observed that CS-2 and CS-3 exhibited highest DPPH (half maximal inhibitory concentration [IC50]: 16.22 and 25.18 μg/mL) and ABTS (IC50: 17.2 and 28.86 μg/mL) radical scavenging activity, respectively, compared to AA (IC50: 15.73 and 16.79 μg/mL) and therefore, both CS-2 and CS-3 were tested for their antidepressant effect using FST and TST as experimental models. Pretreatment of CS-2 and CS-3 (20 mg/kg) for 10 days considerably decreased the immobility time in both the FST and TST models.
CONCLUSION: The antioxidant and antidepressant effect of CS-2 and CS-3 may be attributed to the presence of azomethine linkage in the molecule.
Methods: This study was carried out at the Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia, between June 2016 and July 2017. Bone marrow cells were isolated from nine mice and cultured in a growth medium. Various concentrations of NAC between 0.125-2 μM were added to the culture for 48 hours; these cells were then compared to non-supplemented cells harvested from the remaining three mice as the control group. A trypan blue exclusion test was performed to determine cell viability, while intracellular ROS levels and genotoxicity were determined by hydroethidine staining and comet assay, respectively. The lineage commitment potential of erythroid, myeloid and pre-B-lymphoid progenitor cells was evaluated via colony-forming cell assay.
Results: NAC supplementation at 0.25, 0.5 and 2 μM significantly increased cell viability (P <0.050), while intracellular ROS levels significantly decreased at 0.25 and 0.5 μM (P <0.050). Moreover, DNA damage was significantly reduced at all NAC concentrations (P <0.050). Finally, the potential lineage commitment of the cells was not significantly affected by NAC supplementation (P >0.050).
Conclusion: The findings of this study indicate that NAC supplementation may potentially overcome the therapeutic limitations of ex vivo-maintained HSPCs.
OBJECTIVE: Identify the predictive factors for development of CI-AKI in patients prescribed NAC.
DESIGN: Prospective, cross-sectional.
SETTING: A tertiary hospital in Malaysia.
PATIENTS AND METHODS: All adult patients who were prescribed NAC for prevention of CI-AKI were identified through an NAC drug us.age monitoring card maintained by the inpatient pharmacy. The study was conducted from March to July 2017.
MAIN OUTCOME MEASURES: Statistically significant predictive fac.tors for development of CI-AKI despite NAC administration.
SAMPLE SIZE: 152 RESULTS: The most commonly recognized risk factors for CI-AKI present in the study population were renal impairment (n=131, 86.2%), anemia (n=107, 70.4%), and diabetes mellitus (n=90, 59.2%). Hydration therapy was initiated in 128 patients (84.2%) prior to the contrast-enhanced procedure. Sixty-one (40.1%) were treated with nephrotoxic medications concomitantly with NAC. Fifteen (9.9%) patients developed AKI. Hypotension (OR: 6.02; 95% CI 1.25-28.97) and use of high contrast volume (OR: 6.56; 95% CI: 1.41-30.64) significantly increased the odds for AKI. Prior hydration therapy (OR: 0.13; 95% CI 0.03-0.59) showed protective effects.
CONCLUSION: The risk predictors identified for CI-AKI were hypotension, high contrast volume and prior hydration therapy.
LIMITATION: May not have identified other confounding factors for development of CI-AKI.
CONFLICT OF INTEREST: None.