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Fig. 3. Isocitrate dehydrogenase (IDH) activity of P. microps after 96h of exposure to microplastics (18.4 and 184g L~!), pyrene (20 pgL-'), and combined exposure pyrene and microplastics (20 pgL~! pyrene + 184 pgL~! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene. *Significantly different from the control group (p< 0.05 Dunnett test). The presence of microplastics was found to delay the pyrene-induced mortality: the highest concentration of pyrene (200 wg L~'), in the absence of microplastics, induced 100% mortal- ity after 48h exposure, whereas in the presence of microplastics, the 100% mortality was only recorded after 60h of expo- sure (for both concentrations of plastics). Based on LTs9, the microplastic-induced delay in mortality for treatments contain- ing 200 wgL-! of pyrene was 13.1h for 18.4gL~! and 9.5h for 184 wgL-!. These results suggest toxicologically relevant interac- tions between microplastics and pyrene. Increased accumulation of pyrene metabolites in the bile of fish simultaneously exposed to

Figure 3 Isocitrate dehydrogenase (IDH) activity of P. microps after 96h of exposure to microplastics (18.4 and 184g L~!), pyrene (20 pgL-'), and combined exposure pyrene and microplastics (20 pgL~! pyrene + 184 pgL~! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene. *Significantly different from the control group (p< 0.05 Dunnett test). The presence of microplastics was found to delay the pyrene-induced mortality: the highest concentration of pyrene (200 wg L~'), in the absence of microplastics, induced 100% mortal- ity after 48h exposure, whereas in the presence of microplastics, the 100% mortality was only recorded after 60h of expo- sure (for both concentrations of plastics). Based on LTs9, the microplastic-induced delay in mortality for treatments contain- ing 200 wgL-! of pyrene was 13.1h for 18.4gL~! and 9.5h for 184 wgL-!. These results suggest toxicologically relevant interac- tions between microplastics and pyrene. Increased accumulation of pyrene metabolites in the bile of fish simultaneously exposed to

Related Figures (6)

Fig. 1. Pyrene metabolites in the bile of P. microps after 96h of exposure to microplastics (18.4 and 184ygL~!), pyrene (20gL~'), and combined exposure pyrene and microplastics (20 pgL~! pyrene + 184 zgL-! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene. *Significantly different from the control group (p<0.05 Dunnett test).
Fig. 1. Pyrene metabolites in the bile of P. microps after 96h of exposure to microplastics (18.4 and 184ygL~!), pyrene (20gL~'), and combined exposure pyrene and microplastics (20 pgL~! pyrene + 184 zgL-! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene. *Significantly different from the control group (p<0.05 Dunnett test).
Aortality along time in Pomatoschistus microps juveniles (0+ group) exposed to the different experimental treatments: pyrene 200 p.gL~!; pyrene 200 pg L~! + microplastic 8.4 .gL-!; pyrene 200 pg L-! + microplastics 184 wg L~!. No mortality was recorded during the test in any of the control groups, microplastics treatments without pyren won yrene 20 wg L-! nor pyrene 20 pgL~! + microplastics 184 pg L~!. Pyr — pyrene; MP - microplastics (polyethylene) microspheres; “—” — no mortality. Table 2 Median lethal time (LT59) and 10% lethal time (LTj9) in Pomatoschistus microps juve- niles (0+ group) exposed to pyrene 200 jg L~!; pyrene 200 pg L~! and microplastics 18.4 or 184 pgL-!. 95%CL - 95% confidence limits. Pyr — pyrene; MP - microplastics (polyethylene) microspheres. Table 1
Aortality along time in Pomatoschistus microps juveniles (0+ group) exposed to the different experimental treatments: pyrene 200 p.gL~!; pyrene 200 pg L~! + microplastic 8.4 .gL-!; pyrene 200 pg L-! + microplastics 184 wg L~!. No mortality was recorded during the test in any of the control groups, microplastics treatments without pyren won yrene 20 wg L-! nor pyrene 20 pgL~! + microplastics 184 pg L~!. Pyr — pyrene; MP - microplastics (polyethylene) microspheres; “—” — no mortality. Table 2 Median lethal time (LT59) and 10% lethal time (LTj9) in Pomatoschistus microps juve- niles (0+ group) exposed to pyrene 200 jg L~!; pyrene 200 pg L~! and microplastics 18.4 or 184 pgL-!. 95%CL - 95% confidence limits. Pyr — pyrene; MP - microplastics (polyethylene) microspheres. Table 1
Fig. 2. Acetylcholinesterase activity (AChE) of P. microps after 96h of exposure to microplastics (18.4 and 184gL-'), pyrene (20 gL-'), and combined exposure pyrene and microplastics (20 pg L~! pyrene + 184 pgL-! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene. *Significantly different from the control group (p< 0.05 Dunnett test).
Fig. 2. Acetylcholinesterase activity (AChE) of P. microps after 96h of exposure to microplastics (18.4 and 184gL-'), pyrene (20 gL-'), and combined exposure pyrene and microplastics (20 pg L~! pyrene + 184 pgL-! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene. *Significantly different from the control group (p< 0.05 Dunnett test).
Fig. 5. Lipid peroxidation (LPO) of P. microps after 96h of exposure to microplas- tics (18.4 and 184 pgL~'), pyrene (20 wgL~!), and combined exposure pyrene and microplastics (20 »gL~! pyrene+184ygL7! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene. microplastics and pyrene compared to fish exposed to pyrene alone, seems to support this hypothesis. This may, at least in part, explain the delay of the lethal time observed in fish exposed to the mix- ture treatment relatively to the pyrene single exposure. The fact that the presence of microplastics delayed the lethal time with- out protecting fish from death raises at least two hypotheses, not mutually exclusive: (i) the mechanism involved is transitory and can only be maintained for a relatively short time; (ii) protec- tive mechanisms can only cope with a certain level of internal pyrene/metabolites concentrations, with levels higher than this threshold causing severe toxic effects leading to death. Unfortu- nately, the experimental design in this study does not allow further exploration of this issue. Pyrene and microplastics, either tested individually or in mixture, caused significant reductions in AChE activity, indicating adverse effects in cholinergic neurotransmis- sion and thus potentially in nervous and neuromuscular function. The anticholinesterase properties of pyrene to P. microps were reported in a previous study with older juveniles (2.5-3 cm long) where an inhibition of (42%) of the brain AChE activity was found after 96 h exposure to 500 wg L~! of pyrene (Oliveira et al., 2012). In the present study, younger juveniles of the age 0+ group (1.0-1.2 cm long) showed a significant inhibition of head AChE (19.8%) after 96 h exposure to 20 wg L! of pyrene. To the best of our knowledge, such an ability of microplastics to depress AChE activity has not previously been described. In this study, microplastics alone were
Fig. 5. Lipid peroxidation (LPO) of P. microps after 96h of exposure to microplas- tics (18.4 and 184 pgL~'), pyrene (20 wgL~!), and combined exposure pyrene and microplastics (20 »gL~! pyrene+184ygL7! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene. microplastics and pyrene compared to fish exposed to pyrene alone, seems to support this hypothesis. This may, at least in part, explain the delay of the lethal time observed in fish exposed to the mix- ture treatment relatively to the pyrene single exposure. The fact that the presence of microplastics delayed the lethal time with- out protecting fish from death raises at least two hypotheses, not mutually exclusive: (i) the mechanism involved is transitory and can only be maintained for a relatively short time; (ii) protec- tive mechanisms can only cope with a certain level of internal pyrene/metabolites concentrations, with levels higher than this threshold causing severe toxic effects leading to death. Unfortu- nately, the experimental design in this study does not allow further exploration of this issue. Pyrene and microplastics, either tested individually or in mixture, caused significant reductions in AChE activity, indicating adverse effects in cholinergic neurotransmis- sion and thus potentially in nervous and neuromuscular function. The anticholinesterase properties of pyrene to P. microps were reported in a previous study with older juveniles (2.5-3 cm long) where an inhibition of (42%) of the brain AChE activity was found after 96 h exposure to 500 wg L~! of pyrene (Oliveira et al., 2012). In the present study, younger juveniles of the age 0+ group (1.0-1.2 cm long) showed a significant inhibition of head AChE (19.8%) after 96 h exposure to 20 wg L! of pyrene. To the best of our knowledge, such an ability of microplastics to depress AChE activity has not previously been described. In this study, microplastics alone were
Fig. 4. Glutathione S-transferase (GST) activity of P. microps after 96h of exposure to microplastics (18.4 and 184 .gL~!), pyrene (20 wg L-'), and combined exposure pyrene and microplastics (20 pg L~! pyrene + 184 wgL~! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene.
Fig. 4. Glutathione S-transferase (GST) activity of P. microps after 96h of exposure to microplastics (18.4 and 184 .gL~!), pyrene (20 wg L-'), and combined exposure pyrene and microplastics (20 pg L~! pyrene + 184 wgL~! microplastics). Results are expressed as means + standard errors (n=8). MP - microparticles; Pyr - pyrene.
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