Ercentage of DNA in comet tails, relative to that of unexposed controls as Figure 7. Genotoxic (A) and oxidative (B) DNA damage in Caco-2 cells soon after 24 h and eight weeks of PSNPs exposure, as mean SEM. Statistical significance was DNA damage in Caco-2 cells following 24 h and 8 weeks of comparison post-test. Figure 7. Genotoxic (A) and oxidative (B) determined by one-way ANOVA with Dunnett’s multiplePSNPs exposure, as evidenced by comet assay. Maresin 1 Protocol Information represent the percentage of DNA in comet tails, relative to that of unexposed controls as Comet figures (C) of undamaged cells (left) percentage of DNA in comet tails, relative to that evidenced by comet assay. Data represent the and damaged cell (correct). p 0.01, p 0.001. of unexposed controls as mean SEM. Statistical significance was determined by one-way ANOVA with Dunnett’s various comparison post-test. imply SEM. Statistical significance was determined by one-way ANOVA with Dunnett’s several comparison post-test. Comet figures (C) of undamaged cells (left) and damaged cell (ideal). p 0.01, p 0.001. Comet figures (C) of undamaged cells (left) andROS Production 3.7. Intracellular damaged cell (appropriate). p 0.01, p 0.001.We assessed the intracellular levels of ROS production using the DCFH-DA detection 3.7. Intracellular ROS Production 3.7. Intracellular ROSshow that PSNPs did not induce statistically significant differences in assay. The outcomes Production levels of ROS production together with the DCFH-DA detection We assessed the intracellular We assessed the intracellular levels ofcontrols, neither with the or eight weeks detection ROS levels resultscomparedPSNPs didn’t ROS productionafter 24 h DCFH-DA of exposure assay. The when show that to untreated induce statistically important differences in assay. The results show that PSNPs did notdamage statisticallyor 8 weeks ofcell line, as seen ROS levels when in comparison with untreated controls, neither just after detected within this exposure (Figure 8). Conversely, relevant oxidative induce can be 24 h significant variations in (Figure 8). Conversely, relevant oxidative damage neither right after 24 this cell H2O2. exposure ROS levels when in comparison to untreated controls,can be detected inh or 8 weeks as As a result, these by the enhance in fluorescence in the good handle cells treated withline, of seen by the recommend that PSNPs exposure did control cells treated with Hthis Hence, these (Figure 8). Conversely, relevant oxidative harm can an increase of oxidative tension seen outcomes increase in fluorescence within the positivenot trigger be detected in two O2 . cell line, as within the by final results recommend that PSNPs exposure did not trigger a rise of oxidative stressThus, these the boost in samples. PSNPs-exposed fluorescence inside the positive control cells treated with H2O2. within the PSNPs-exposed samples. final results suggest that PSNPs exposure did not bring about a rise of oxidative pressure within the PSNPs-exposed samples.Figure 8. Presence of intracellular ROS levels as detected by DCFH-DA fluorescence assay in cells exposed to exposed to PSNPs for 24 h h andweeks, untreated controls, and good controls treated with H2 O2 . PSNPs for 24 and 8 8 weeks, untreated controls, and positive controls treated with the percentage of fluorescence intensity relative towards the optimistic control is shown. Data are represented H2O 8. Presence of intracellular ROS intensity relative by DCFH-DA control is shown. Data are Figure2. The percentage of fluorescencelevels as detected to the optimistic fluorescenc.