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Biomedical subjects

J Pinto

Publications and source records attributed to J Pinto.

At least 109 records · Page 6Linked to original sources
PubMed1978

Increased urinary riboflavin excretion resulting from boric acid ingestion.

The urinary excretion of riboflavin (vitamin B2) was determined in 14 patients, both children and adults, after the ingestion of boric acid. These patients reported to the New York City Poison Control Center during a 2 1/2 year period. Riboflavin was determined by a modification of a previously described method which is based upon competitive protein binding. Boric acid ingestion was associated with greatly increased urinary riboflavin excretion in approximately two thirds of the patients. Most of the riboflavin appeared to be excreted within the first 24 hr after ingestion of boric acid. These data provide evidence of a previously unrecognized hazard of boric acid ingestion in patients.

Acute Disease↗
PubMed1977

Enhanced riboflavin incorporation into flavins in newborn riboflavin-deficient rats.

The incorporation of a subcutaneous injection of [14C]riboflavin (2.5 muCi/100 g body wt) into flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD), and flavins bound covalently to proteins was determined at 1, 6, and 18 h in liver, cerebrum, and cerebellum from progeny of normal and maternally riboflavin-deficient Holtzman rats. Radioactivity remaining as riboflavin was also determined under these circumstances. Experiments were initiated within 24 h of birth. In both groups of newborn rats, the incorporation of radioactive riboflavin into covalently bound flavins in liver and brain proceeded more slowly than into the other flavin fractions. In addition, radioactivity incorporated into covalently bound flavins comprised a relatively smaller proportion of the total amount incorporated in brain than in liver. In progeny of riboflavin-deficient dams, an increased rate of incorporation of riboflavin into all three flavin derivatives, particularly FAD, was observed in liver and brain, compared to results in normal progeny. These data provide evidence that maternal riboflavin deficiency enhances the incorporation of riboflavin into tissue flavins in liver, cerebrum, and cerebellum from newborn rats.

Animals↗