Brunella Tolomelli

Vitamin B6 deficiency affects antioxidant defences in rat liver and heart

We have evalued the effects of a diet containing normal amounts of lipids and a marginal content of vitamin B6 on lipid peroxidation. Pyridoxal phosphate concentrations of plasma and liver indicated that an initial deficiency state was reached. Vitamin B6 deficiency led to peroxidative stress: TBARS production was higher in the liver (+18·6%) and even more in the heart (+61%) of deficient rats as compared with controls. Furthermore, significant stimulation of glutathione‐dependent enzymes occurred in both heart and liver of deficient rats: glutathione peroxidase activity increased in heart (+144%) and liver (+505%); glutathione reductase increased in heart (+54·9%) and liver (+15·5%). No difference in the total glutathione content of the organs of the two groups was observed. The reduced glutathione/oxidized glutathione ratio was significantly lower in deficient rats. Although the activity of glutathione‐dependent enzymes was significantly greater in deficient rats than in controls, this stimulation was only partially able to counteract the peroxidative damage due to vitamin B6 deficiency.

Studies on the Folate Coenzyme Metabolism in the Castrated Rat and Treated with 17β-Estradiol

Summary The effect of 17β-estradiol on folate coenzyme metabolism was studied in normal and castrated female rats. The capacity of conversion in vivo of folic acid into activated forms was investigated by measuring the quantity of folate derivatives in the urine and the liver folate coenzyme contents after injection of folic acid. An increase in the urinary excretion of folate metabolites and a decrease in the liver content of reduced folate forms in castrated rats was seen compared with normal rats. Treatment of castrated animals with 17β-estradiol were corrective. The enzymic activities involved in the folate coenzyme metabolism were assayed in vitro both in the liver and in the uterus. Severe alterations were observed in the enzymes of castrated animals and here, too, 17β-estradiol administration restored the biochemical lesions almost completely. The results show a possible influence on folate coenzyme synthesis by 17β-estradiol.

Effects of testosterone on folate coenzymes in the rat.

Summary In the liver of castrated rats a significant decrease of total folate coenzymes and, in particular, of 10-HCO-H4folate and H4folate was observed. Treatment with testosterone normalizes the folate content of these structures. The decrease in folate coenzymes is evident in the prostate but here too, hormone administration restores the normal folate content. Castration does not significantly alter the content or distribution of folate coenzymes in seminal vesicles. We are indebted to Mr. Roberto Laffi for excellent technical assistance.

Distribution of Pteroylglutamates in Developing Chick Embryo

Abstract Distribution of poly- and monoglutamate forms of folate coenzymes was studied in the whole egg, the nonembryonic portion of the egg, and in the embryo at various stages of development. Total folate activity of the nonembryonic portion decreases significantly after 12 days of incubation, while the folate activity of the embryo gradually increases. In the nonembryonic portion of the egg folates are present in monoglutamate form. The embryo assumes monoglutamates and immediately synthetises polyglutamates. In fact, these compounds are the only folate forms present in embryo and they increase progressively during development.

Distribution of Pteroylglutamates during Liver Regeneration after Partial Hepatectomy in Folic Acid-Deficient Rats

Abstract Normal and folate-deficient rats were partially hepatectomized and sacrificed at various times after the operation. The distribution of pteroylmono- and polyglutamates was evaluated by Sephadex G-15 chromatography and microbiological assay. The incorporation of thymidine into DNA was also studied. Deficient rats show a fall in penta-and hexaglutamates and intermediate forms beginning 12 hr after the operation. Monoglutamates diminished but less than the other compounds. In control rats the higher polyglutamates after an initial decrease rise to normal values at 180 hr; the intermediate forms had already increased at 12 hr and remained high at the following times and monoglutamates at first decreased but at 180 hr exceeded normal values. The rate of DNA synthesis is not only decreased, but also delayed in regenerating liver of deficient rats as compared with controls. The livers of deficient rats appear unable to synthesize adequate quantities of polyglutamates. This fact may explain the slowing down of the regenerative process in folic acid-deficient rats, demonstrated by lower and delayed thymidine incorporation into DNA.

Diurnal Variations of Liver Folate Metabolism in Rats Maintained Under Controlled Feeding Schedules

Summary Rats maintained under controlled feeding schedules exhibit daily rhythms of the enzyme activities involved in folate metabolism. Tetrahydrofolate dehydrogenase and serine hydroxymethyl transferase show only small variations in their activity in the range of the 24-hr cycle. The 5,10-CH2-H4folate dehydrogenase shows a peak of activity at 6 PM (18:00), while the 5,10-CH2-H4folate synthetase activity reaches its lowest level between 3:00 PM (15:00) and 3:00 AM (3:00). The liver content of folate coenzymes does not change significantly during the whole day.