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 following 24 h and 8 weeks of PSNPs exposure, as imply 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. 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 broken cell (suitable). 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. mean SEM. Statistical significance was determined by one-way ANOVA with Dunnett’s various comparison post-test. Comet figures (C) of undamaged cells (left) and damaged cell (appropriate). p 0.01, p 0.001. Comet figures (C) of undamaged cells (left) andROS Production 3.7. Intracellular damaged cell (right). p 0.01, p 0.001.We assessed the intracellular levels of ROS production with all the DCFH-DA detection 3.7. Intracellular ROS Production three.7. Intracellular ROSshow that PSNPs did not induce statistically important variations 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 8 weeks detection ROS levels resultscomparedPSNPs didn’t ROS productionafter 24 h DCFH-DA of exposure assay. The when show that to untreated induce statistically considerable variations in assay. The results show that PSNPs did notdamage statisticallyor 8 weeks ofcell line, as observed ROS levels when in comparison with untreated controls, neither right after detected within this exposure (Figure eight). Conversely, relevant oxidative induce is usually 24 h important differences in (Figure eight). Conversely, relevant oxidative harm neither soon after 24 this cell H2O2. exposure ROS levels when in comparison with untreated controls,can be detected inh or 8 weeks as Therefore, these by the raise in fluorescence in the positive manage cells treated withline, of noticed by the recommend that PSNPs exposure did manage cells treated with Hthis As a result, these (Figure 8). Conversely, relevant oxidative damage can a rise of oxidative Hematoporphyrin Autophagy anxiety noticed benefits boost in fluorescence within the positivenot lead to be detected in two O2 . cell line, as within the by final results suggest that PSNPs exposure did not lead to a rise of oxidative stressThus, these the increase in samples. PSNPs-exposed fluorescence within the constructive manage cells treated with H2O2. in the PSNPs-exposed samples. outcomes recommend that PSNPs exposure did not result in an increase of oxidative strain within the PSNPs-exposed samples.Figure eight. Allyl methyl sulfide Autophagy 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 optimistic controls treated with H2 O2 . PSNPs for 24 and eight eight weeks, untreated controls, and constructive controls treated with the percentage of fluorescence intensity relative towards the optimistic handle is shown. Information are represented H2O 8. Presence of intracellular ROS intensity relative by DCFH-DA manage is shown. Data are Figure2. The percentage of fluorescencelevels as detected for the positive fluorescenc.