Key result
Grass carp bile inhibits renal dipeptidase and increases nitrite ~52%, suggesting nitric oxide drives bile-induced renal failure.
Why the study?
Acute renal failure after ingestion of grass carp bile is reported, but the mechanisms involving renal dipeptidase release and nitric oxide generation are unclear.
Grass carp bile inhibits the release of renal dipeptidase from proximal tubules via nitric oxide generation and the phospholipase C pathway, potentially explaining its role in acute renal failure.
Answers are grounded in this paper and cite their sources.
Supports nitric oxide-mediated tubular effects in vitro; hypothesis-generating for human bile-induced acute kidney injury.
There are many reports on acute renal failure (ARF) after ingestion of grass carp bile (CB; Ctenopharyngodon idellus). Renal dipeptidase (RDPase; EC 3.4.13.19) is a glycosylphosphatidylinositol-anchored ectoenzyme within the renal proximal tubules (PTs) and is proposed as a diagnostic enzyme of renal disease. We examined the release of RDPase following treatment with CB and various nitric oxide (NO) related compounds in porcine PTs. The RDPase release from PTs was inhibited by CB in a concentration-dependent manner and was also inhibited by sodium nitroprusside (direct NO donor) and L-arginine (NO synthase substrate) in the tested range (0-12 mM). CB-treated (0. 1 mg/ml) PTs showed a decreased RDPase activity in comparison with the control group. This inhibition was blocked by 2 mM L-NAME (NO synthase inhibitor) and U73122 (inhibitor of phosphatidylinositol-specific phospholipase C) in a concentration-dependent manner. Eel bile (0-0.1 mg/ml), used as the control, did not significantly affect the RDPase release from PTs. The NO concentration was observed as nitrite, the degradation product of the NO metabolism, increased in proportion to CB and L-arginine. The increase of nitrite to 151.5% by CB treatment (0.1 mg/ml) was blocked by 2 mM L-NAME (95.5%). When the phospholipase C pathway was blocked by 10 and 20 microM U73122, the nitrite generation decreased to 122.7 and 89.4%, respectively. These results strongly suggest that NO generation and the phospholipase C pathway affect the RDPase release from the PTs and that they may be involved in the development of ARF in vivo following CB ingestion. The release of RDPase from PTs could be a useful tool not only for this CB-caused ARF, but also for the elucidation of other biochemical mechanisms.
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Choi et al. (2000) studied Acute renal failure. Grass carp bile vs. Eel bile or control was evaluated on Release of renal dipeptidase (RDPase) and nitrite generation. Grass carp bile inhibited the release of renal dipeptidase from porcine proximal tubules and increased nitrite generation to 151.5%, suggesting nitric oxide's role in bile-induced acute renal failure.
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