Understanding the mechanisms by which individual organisms respond and populations adapt to global climate change is a critical challenge. The role of plasticity and acclimation, within and across generations, may be essential given the pace of change. We investigated plasticity across generations and life stages in response to ocean acidification (OA), which poses a growing threat to both wild populations and the sustainable aquaculture of shellfish. Most studies of OA on shellfish focus on acute effects, and less is known regarding the longer term carryover effects that may manifest within or across generations. We assessed these longer term effects in red abalone (
Combined environmental stressors that an organism experiences can have both immediate and lasting consequences. In the present study, we exposed Japanese medaka (
- NSF-PAR ID:
- 10447323
- Publisher / Repository:
- Wiley Blackwell (John Wiley & Sons)
- Date Published:
- Journal Name:
- Environmental Toxicology and Chemistry
- Volume:
- 41
- Issue:
- 3
- ISSN:
- 0730-7268
- Page Range / eLocation ID:
- p. 748-757
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Abstract Haliotis rufescens ) using a multi‐generational split‐brood experiment. We spawned adults raised in ambient conditions to create offspring that we then exposed to high pCO2(1180 μatm; simulating OA) or low pCO2(450 μatm; control or ambient conditions) during the first 3 months of life. We then allowed these animals to reach maturity in ambient common garden conditions for 4 years before returning the adults into high or low pCO2treatments for 11 months and measuring growth and reproductive potential. Early‐life exposure to OA in the F1 generation decreased adult growth rate even after 5 years especially when abalone were re‐exposed to OA as adults. Adult but not early‐life exposure to OA negatively impacted fecundity. We then exposed the F2 offspring to high or low pCO2treatments for the first 3 months of life in a fully factorial, split‐brood design. We found negative transgenerational effects of parental OA exposure on survival and growth of F2 offspring, in addition to significant direct effects of OA on F2 survival. These results show that the negative impacts of OA can last within and across generations, but that buffering against OA conditions at critical life‐history windows can mitigate these effects. -
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Key points Vascular oxidative stress increases with advancing age.
We hypothesized that resistance vessels develop resilience to oxidative stress to protect functional integrity and tested this hypothesis by exposing isolated pressurized superior epigastric arteries (SEAs) of old and young mice to H2O2.
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Vascular cells develop resilience to H2O2during ageing by preventing Ca2+overload and endothelial integrity promotes SMC survival.
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m , 50 min). Mouse superior epigastric arteries (SEAs; diameter, ∼150 µm) were isolated and pressurized to 100 cmH2O at 37˚C. For SEAs from young (4 months) mice, H2O2killed 57% of SMCs and 11% of ECs in malesvs . 8% and 2%, respectively, in females. Therefore, SEAs from males were studied to resolve the effect of ageing and experimental interventions. For old (24 months) mice, SMC death was reduced to 10% with diminished accumulation of [Ca2+]iin the vessel wall during H2O2exposure. In young mice, genetic deletion of IL‐10 mimicked the protective effect of ageing on cell death and [Ca2+]iaccumulation. Whereas endothelial denudation or gap junction inhibition (carbenoxolone; 100 µm ) increased SMC death, inhibiting NO synthase (l ‐NAME, 100 µm ) or scavenging peroxynitrite (FeTPPS, 5 µm ) reduced SMC death along with [Ca2+]i. Despite NO toxicity via peroxynitrite formation, endothelial integrity protects SMCs. Caspase inhibition (Z‐VAD‐FMK, 50 µm ) attenuated cell death with immunostaining for annexin V, cytochrome C, and caspases 3 and 9 pointing to induction of intrinsic apoptosis during H2O2exposure. We conclude that advanced age reduces Ca2+influx that triggers apoptosis, thereby promoting resilience of the vascular wall during oxidative stress. -
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Abstract Larvae of marine calcifying organisms are particularly vulnerable to the adverse effects of elevated
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