NOSTRIN

Seed priming by nitric oxide (NO) and hydrogen sulphide (H₂S) in combating against abiotic stress in plants is well documented. However, knowledge of fundamental mechanisms of their crosstalk is scrambled. Therefore, the reported study examined the probable role of NO and H₂S in the mitigation of arsenate toxicity (As(V)) in rice seedlings and whether their potential signalling routes crossover. Results report that As(V) toxicity limited shoot and root length growth with more As accumulation in roots. As(V) further caused elevated reactive oxygen species levels, inhibited ascorbate-glutathione cycle enzymes and relative gene expression of its enzymes and thus, causing lipid and protein oxidation. These results correlate with reduced nitric oxide synthase-like and _L-cysteine desulfhydrase activity along with endogenous NO and H₂S. While, L-NAME or PAG augmented As(V) toxicity, and addition of SNP or NaHS effectively reversed their respective effects. Furthermore, SNP under PAG or NaHS under L-NAME were able to pacify As(V) stress, implicating that endogenous NO and H₂S efficiently ameliorate As(V) toxicity but without their shared signaling in rice seedlings.

Decreased nitric oxide (NO) bioavailability in a cirrhotic liver contributes to high intrahepatic vascular resistance (IHVR) and portal hypertension (PHT). Nostrin is an inhibitory protein of NO synthesising enzyme endothelial NO synthase (eNOS), shown to increase in cirrhosis with PHT, however, the precise molecular mechanism is poorly documented. This study aimed to elucidate the role of Nostrin and associated derangement in hepatic NO generation in cirrhotic liver. Further, we investigate whether Nostrin could be a biomarker in the progression of cirrhosis.

This study was conducted on sixty healthy subjects and 120 cirrhotic patients. In addition, liver tissue samples were collected from cirrhotic patients for the analysis of Nostrin, eNOS and inflammatory markers.

When compared to healthy controls, systemic levels of Nostrin and cGMP were elevated in compensated cirrhosis. In decompensated cirrhosis, further robust increases in Nostrin and cGMP were noted. Furthermore, Nostrin expression was considerably higher whilst reduced eNOS activity and hepatic cGMP levels in cirrhotic liver compared to control liver.

In cirrhotic patients, a robust increase in hepatic Nostrin expression may reduce eNOS activity and associated local NO generation. Furthermore, Blood Nostrin concentration was higher and parallel to disease severity and could be a key diagnostic and prognostic biomarker in cirrhotic patients with PHT.