Modeling of CO2-LPG WAG with asphaltene deposition to predict coupled enhanced oil recovery and storage performance.

Combined carbon capture and storage and CO2-enhanced oil recovery (CCS-EOR) can reconcile the demands of business with the need to mitigate the effects of climate change. To improve the performance of CCS-EOR, liquefied petroleum gas (LPG) can be co-injected with CO2, leading to a reduction in the minimum miscibility pressure. However, gas injection can cause asphaltene problems, which undermines EOR and CCS performances simultaneously. Here, we systematically examine the mechanisms of asphaltene deposition using compositional simulations during CO2-LPG-comprehensive water-alternating-gas (WAG) injection. The LPG accelerates asphaltene deposition, reducing gas mobility, and increases the performance of residual trapping by 9.2% compared with CO2 WAG. In contrast, solubility trapping performance declines by only 3.7% because of the greater reservoir pressure caused by the increased formation damage. Adding LPG enhances oil recovery by 11% and improves total CCS performance by 9.1% compared with CO2 WAG. Based on reservoir simulations performed with different LPG concentrations and WAG ratios, we confirmed that the performance improvement of CCS-EOR associated with increasing LPG and water injection reaches a plateau. An economic evaluation based on the price of LPG should be carried out to ensure practical success.

Acrolein, the toxic endogenous aldehyde, induces neurofilament-L aggregation.

Acrolein is a highly reactive by product of lipid peroxidation and individuals with neurodegenerative disorders have been shown to contain elevated concentrations of this molecule in the brain. In the present study, we examined the pattern of neurofilament-L (NF-L) modification elicited by acrolein. When NF-L was incubated with acrolein, protein aggregation occurred in a acrolein concentration-dependent manner. Exposure of NF-L to acrolein also led to the generation of protein carbonyl compounds. Through the addition of free radical scavengers we observed a significant decrease in acrolein-mediated NF-L aggregation. These results indicate that free radicals may be involved in the modification of NF-L by acrolein. In addition, dityrosine crosslink formation was observed in acrolein-mediated NF-L aggregates and these aggregates displayed thioflavin T reactivity, reminiscent of amyloid. This study suggests that acrolein-mediated NF-L aggregation might be closely related to oxidative reactions, thus these reactions may play a critical role in neurodegenerative diseases.

Oxidative modification of cytochrome c by hydrogen peroxide.

Oxidative alteration of mitochondrial cytochrome c has been linked to disease and is one of the causes of pro-apoptotic events. We have investigated the modification of cytochrome c by H2O2. When cytochrome c was incubated with H2O2, oligomerization of the protein increased and the formation of carbonyl derivatives and dityrosine was stimulated. Radical scavengers prevented these effects suggesting that free radicals are implicated in the H2O2-mediated oligomerization. Oligomerization was significantly inhibited by the iron chelator, deferoxamine. During incubation of deoxyribose with cytochrome c and H2O2, damage to the deoxyribose occurred in parallel with the release of iron from cytochrome c. When cytochrome c that had been exposed to H2O2 was analyzed by amino acid analysis, the tyrosine, histidine and methionine residues proved to be particularly sensitive. These results suggest that H2O2-mediated cytochrome c oligomerization is due to oxidative damage resulting from free radicals generated by a combination of the peroxidase activity of cytochrome c and the Fenton reaction of free iron released from the oxidatively-damaged protein.

Oxidative modification of neurofilament-L by the Cu,Zn-superoxide dismutase and hydrogen peroxide system.

Neurofilament-L (NF-L) is a major element of neuronal cytoskeletons and known to be important for their survival in vivo. Since oxidative stress might play a critical role in the pathogenesis of neurodegenerative diseases, we investigated the role of Cu,Zn-superoxide dismutase (SOD) in the modification of NF-L. When disassembled NF-L was incubated with Cu,Zn-SOD and H2O2, the aggregation of protein was proportional to the concentration of hydrogen peroxide. Cu,Zn-SOD/H2O2-mediated modification of NF-L was significantly inhibited by radical scavenger, spin trap agents and copper chelators. Dityrosine crosslink formation was obtained in Cu,Zn-SOD/H2O2-mediated NF-L aggregates. Antioxidant molecules, carnosine and anserine significantly inhibited the aggregation of NF-L and the formation of dityrosine. This study suggests that copper-mediated NF-L modification may be closely related to oxidative reactions which play a critical role in neurodegenerative diseases.