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Elucidating the Role of the Metal Catalyst and Oxide Support in the Ru/CeO₂-Catalyzed CO₂ Methanation Mechanism.

ABSTRACT: This study addresses the yet unresolved CO₂ methanation mechanism on a Ru/CeO₂ catalyst by means of near-ambient-pressure X-ray photoelectron spectroscopy (NAP-XPS) and diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) complemented with periodic density functional theory (DFT) calculations. NAP-XPS results show that the switch from H₂ to CO₂ + H₂ mixture oxidizes both the Ru and CeO₂ phases at low temperatures, which is explained by the CO₂ adsorption modes assessed by means of DFT on each representative surface. CO₂ adsorption on Ru is dissociative and moderately endergonic, leading to polybonded Ru-carbonyl groups whose hydrogenation is the rate-determining step in the overall process. Unlike on Ru metal, CO₂ can be strongly adsorbed as carbonates on ceria surface oxygen sites or on the reduced ceria at oxygen vacancies as carboxylates (CO₂ ^-δ), resulting in the reoxidation of ceria. Carboxylates can then evolve as CO, which is released either via direct splitting at relatively low temperatures or through stable formate species at higher temperatures. DRIFTS confirm the great stability of formates, whose depletion relates with CO₂ conversion in the reaction cell, while carbonates remain on the surface up to higher temperatures. CO generation on ceria serves as an additional reservoir of Ru-carbonyls, cooperating to the overall CO₂ methanation process. Altogether, this study highlights the noninnocent role of the ceria support in the performance of Ru/CeO₂ toward CO₂ methanation.

SUBMITTER: Lopez-Rodriguez S

PROVIDER: S-EPMC8631708 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundTo better assess potential hepatotoxicity of nanomaterials, human liver HepG2 cells were exposed for 3 days to five different CeO2 (either 30 or 100 μg/ml), 3 SiO2 based (30 μg/ml) or 1 CuO (3 μg/ml) nanomaterials with dry primary particle sizes ranging from 15 to 213 nm. Metabolomic assessment of exposed cells was then performed using four mass spectroscopy dependent platforms (LC and GC), finding 344 biochemicals.ResultsFour CeO2, 1 SiO2 and 1 CuO nanomaterials increased hepatocyte concentrations of many lipids, particularly free fatty acids and monoacylglycerols but only CuO elevated lysolipids and sphingolipids. In respect to structure-activity, we now know that five out of six tested CeO2, and both SiO2 and CuO, but zero out of four TiO2 nanomaterials have caused this elevated lipids effect in HepG2 cells. Observed decreases in UDP-glucuronate (by CeO2) and S-adenosylmethionine (by CeO2 and CuO) and increased S-adenosylhomocysteine (by CuO and some CeO2) suggest that a nanomaterial exposure increases transmethylation reactions and depletes hepatic methylation and glucuronidation capacity. Our metabolomics data suggests increased free radical attack on nucleotides. There was a clear pattern of nanomaterial-induced decreased nucleotide concentrations coupled with increased concentrations of nucleic acid degradation products. Purine and pyrimidine alterations included concentration increases for hypoxanthine, xanthine, allantoin, urate, inosine, adenosine 3',5'-diphosphate, cytidine and thymidine while decreases were seen for uridine 5'-diphosphate, UDP-glucuronate, uridine 5'-monophosphate, adenosine 5'-diphosphate, adenosine 5'-monophophate, cytidine 5'-monophosphate and cytidine 3'-monophosphate. Observed depletions of both 6-phosphogluconate, NADPH and NADH (all by CeO2) suggest that the HepG2 cells may be deficient in reducing equivalents and thus in a state of oxidative stress.ConclusionsMetal oxide nanomaterial exposure may compromise the methylation, glucuronidation and reduced glutathione conjugation systems; thus Phase II conjugational capacity of hepatocytes may be decreased. This metabolomics study of the effects of nine different nanomaterials has not only confirmed some observations of the prior 2014 study (lipid elevations caused by one CeO2 nanomaterial) but also found some entirely new effects (both SiO2 and CuO nanomaterials also increased the concentrations of several lipid classes, nanomaterial induced decreases in S-adenosylmethionine, UDP-glucuronate, dipeptides, 6-phosphogluconate, NADPH and NADH).

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Elucidating the Role of the Metal Catalyst and Oxide Support in the Ru/CeO₂-Catalyzed CO₂ Methanation Mechanism.

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Elucidating the Role of the Metal Catalyst and Oxide Support in the Ru/CeO2-Catalyzed CO2 Methanation Mechanism.

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Elucidating the Role of the Metal Catalyst and Oxide Support in the Ru/CeO₂-Catalyzed CO₂ Methanation Mechanism.