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SUMMARY Acetate disappearance from the loops of the hindgut in the rabbit was evaluated by measuring variations in the concentration of acetate in caecocolonic loops and differences in the arterial and venous plasma. In vivo metabolism in gut and liver tissues was studied after introduction of (1-'4C) acetate into caecocolonic loops.

Abstract— Photobinding of sulfanilamide to bovine serum albumin (BSA) was investigated by irradiating BSA and buffered BSA/drug solutions with UV light (Λ= 300 nm) under anaerobic conditions. The protein solutions were then denatured and the unbound sulfanilamide removed. Marked differences in the UV and fluorescence spectra of the solutions before and after irradiation were observed, suggesting covalent binding of the drug to BSA. This was confirmed using [14C]labelled sulfanilamide. The extent of photobinding of sulfanilamide determined using the radiolabeled drug, was concentration dependent. The binding ratio varied from 3 mol drug per mol BSA for a 10‐4M drug concentration, to 10 mol drug per mol BSA for 10‐2M drug concentration. The protein solutions were hydrolysed under acid conditions and the amino acids obtained were analysed by ion exchange chromatography. The hydrolysate of irradiated BSA (10‐4M) ‐sulfanilamide (10‐2M) mixture lost about 10 mol of cystine per mol of BSA. This loss was not observed after hydrolysis of irradiated alone or non‐irradiated BSA. Irradiation of cystine with [14C]sulfanilamide in HC1 solutions produced the same compound as was found after hydrolysis of irradiated BSA/sulfanilamide mixtures. This was demonstrated by autoradiography of paper chromatograms. The same compound was also detected in an irradiated [35S]cystine non‐labelled sulfanilamide mixture. It was not detected, however, after irradiation of a mixture of all amino acids of BSA excluding cystine. These data suggest that cystine residues are involved in the photobinding of sulfanilamide (or its photoproducts) to BSA.

We report the case of a 56-year-old woman with a history of episodes of vomiting and coma. Hyperammoniemia, hypouremia, hypercitrullinemia and the decreased arginino-succinic synthetase activity on skin fibroblast cultures permitted us to diagnose citrullinemia. We think that the skin changes, i.e. atrophy of the epidermis, thin and short collagen bundles, dystrophic elastic fibers, increased fundamental matrix, were due to the undernutrition state and were not specific. The dosage of the amino acids of the total skin showed a decreased hydroxylation of lysine in the insoluble fraction, and the presence of pro-line and hypdroxyproline in the soluble fraction. These metabolic changes were not specific and evidenced the disorganization and the lysis of the connective tissue due to the undernutritional state. The nail changes, i.e. clubbed fingers and ‘half-and-half nail’ syndrome, were not specific either. The hair changes mentioned by other authors in newborns and young children, i.e. sparse and brittle blond hair, presence of transverse opaque bands (‘irregularly banded hair’), were not present in our case. We only found changes in the cuticle and some trichorrhexis which were not specific of the disease either.