AI Article Synopsis
- Sulfur dioxide (SO2) is produced by an enzyme called glutamate-oxaloacetate transaminase (GOT) from L-cysteine in mammalian cells, and this study explores its role in inflammation related to acute lung injury (ALI) after limb ischemia/reperfusion (I/R).
- In an experiment with male Wistar rats, it was found that limb I/R significantly reduced plasma SO2 levels and GOT activity in lung tissue, indicating a potential link between SO2 and inflammation in ALI.
- Treatment with SO2 donor compounds could prevent ALI, while inhibiting GOT worsened the condition, suggesting that reduced SO2 production may contribute to the development of ALI following limb I/R
Article Abstract
Sulfur dioxide (SO2) is naturally synthesized by glutamate-oxaloacetate transaminase (GOT) from L-cysteine in mammalian cells. We aim to investigate the role of SO2 in inflammation in acute lung injury (ALI) following limb ischemia/reperfusion (I/R). Male Wistar rats were subjected to limb I/R and were injected with saline, GOT inhibitor hydroxamate (HDX, 0.47 mmol/kg), or the SO2 donor Na2 SO3 /NaHSO3 (0.54 mmol/kg/0.18 mmol/kg). Compared with the sham operation, the plasma SO2 levels were significantly decreased by limb I/R treatment. In addition, SO2 concentration and GOT activity in the lung tissue were also reduced in ALI. The occurrence of ALI following limb I/R can be prevented by Na2 SO3 /NaHSO3 treatment, whereas it can be significantly aggravated by HDX. The plasma IL-1β, IL-6, and IL-10 levels were consistent with myeloperoxidase activity and inflammation in lung tissue. In conclusion, our data suggest that downregulation of endogenous SO2 production might be involved in pathogenesis of ALI following limb I/R in rats.
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| http://dx.doi.org/10.1002/jbt.21492 | DOI Listing |
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