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S Ronca-Testoni

Publications and source records attributed to S Ronca-Testoni.

62 records · Page 4Linked to original sources
PubMed1968

The effect of chemical modifications induced in insulin on the reactivity of the interchain disulphide bonds towards sodium sulphite.

The reactivity of the three disulphide bridges of insulin towards sodium sulphite was studied by amperometric titration of the liberated thiol groups. In the native, acetylated or succinylated molecule two bridges react at pH7, but in the methylated or phenylcarbamoylated molecule only one bridge reacts. All three bridges react in all derivatives in 8m-urea or at pH9. Loss in biological activity parallels the loss in reactivity of one of the bridges during methylation. It is suggested that change in reactivity of the S.S bonds reflects the occurrence of a conformational modification of the protein. The possibility is discussed that the unusually high reactivity of the S.S bonds in native insulin depends strictly on the integrity of the native molecule, suggesting that S.S bonds are in some way involved in the hormone's mode of action.

Acetates↗
PubMedDate not supplied

Determination of adenosine kinase activity by high-pressure liquid chromatography.

High-pressure liquid chromatography (reverse-phase mode) was used to assay adenosine kinase in cell and tissue extracts. The method is optimized for a rapid and selective analysis using 6-methylthiopurine riboside as substrate, isocratic elution and detection at 300 nm. A complete separation of substrate and product is achieved in about 3 min with no interference by other UV-absorbing compounds; the limit of detection is 20 pmoles.

Adenosine Kinase↗
PubMedDate not supplied

Release of uric acid from perfused rat heart.

The release of purine compounds from the perfused rat heart under basal conditions was determined by high pressure liquid chromatography. Uric acid resulted the major degradative released into the perfusate. Lower levels of hypoxanthine, xanthine and inosine were found. The uric acid concentration showing that the rat heart is able to catabolize the purine compounds up to uric acid. No leakage of catabolic enzymes was observed and thereby the breakdown of the released nucleosides and bases proved to be intracellular. This heart ability was confirmed by the analysis of the degradation products of AMP added to the perfusion medium in the recirculating system. AMP was sequentially broken down to adenosine, then to inosine, hypoxanthine and xanthine and finally to uric acid that as end product accumulated in the perfusate.

Adenosine Monophosphate↗