Upon on-off RF field exposure, a significant decrease in tumor cell viability is observed, suggesting successful drug release into the tumor site.
After 120 h exposure, a significant decrease was observed at low concentration (p = 0.032) and no significant changes were observed with the high concentration, but the percentage of change was below the control.
In biochemical indices, after 23-day exposure, a significant decrease in glucose, cholesterol (P < 0.05), and ammonia (P < 0.01) was recorded in the experimental group compared to the control group.
Both the 100%and5050% NPE/OPE exposures caused a significant decrease in reproductive behavior, as indicated by an inability of many of the previously exposed males to acquire and hold a nest site required for reproduction.
Our findings that these exposures caused a significant decrease in proteasome activity suggests a novel biochemical pathway that may be important in the pathophysiologic response to air pollutants.
In Figure 5A, Aβ exposure yielded a significant decrease in the microglial mitochondrial red/green fluorescence intensity ratio at 6 hours following Aβ exposure when compared to untreated control microglia, suggesting that Aβ exposure results in mitochondrial membrane depolarization.
In both treated groups, Al exposure induced a significant decrease of locomotor performance.
AMP exposure induced a significant decrease in cell viability and a significant increase in the leakage of hepatic enzymes {lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and asparate aminotransferase (AST)} in a concentration and time-related manner.
In contrast, PFOS exposure evoked a significant decrease in cytosolic PKC, primarily for the β and γ isoforms, but again without a corresponding change in membrane-associated enzyme; this likely partial, compensatory increases in translocation to offset the net PKC deficiency.
By 35 and 50 days, BBP exposure induced a significant decrease in the expression of Gad1.
