Dual influence of aging and vitamin B6 deficiency on delta-6-desaturation of essential fatty acids in rat liver microsomes.

Delta-6-desaturase (D6D) activity is influenced by many nutritional and non-nutritional factors, among which one of the most important is aging. D6D activity could be susceptible to the dual influence of aging itself and of nutritional deficiencies, due to the reduced intake and/or absorption of essential nutrients. Particularly, vitamin B6 deficiency might be a crucial factor for D6D activity in aged people. Using 20 month old Sprague-Dawley rats fed a diet with a subnormal level of vitamin B6, we evaluated D6D activity for linoleic acid (LA) and alpha-linolenic acid (ALA) in liver microsomes, and the fatty acid composition of microsomal total lipids. We observed a diminished D6D activity for LA and also for ALA in vitamin B6-deficient animals, being approximately 63% and 81% respectively of the corresponding activity in control rats. As a consequence, significant modifications in the relative molar content of microsomal fatty acids were observed. The content of arachidonic and docosahexaenoic acid, the main products of the conversion of LA and ALA respectively, decreased, LA content increased and a decrease in the unsaturation index was observed in liver microsomes of B6-deficient rats. The foregoing results suggest that the impairment of D6D activity by vitamin B6 deficiency might be an important factor in decreasing the synthesis of n-6 and n-3 PUFAs. This may be particularly important in aging, where D6D activity is already impaired.

Effects of short-term dietary administration of marginal levels of vitamin B(6)and fish oil on lipid composition and antioxidant defences in rat tissues.

Previous reports have shown that vitamin B(6)deficiency leads to peroxidative stress in rat organs. In this paper, we evaluated the effects on lipid peroxidation of short-term (six weeks) dietary administration of marginal contents of vitamin B(6). A further risk factor of susceptibility to peroxidation was the presence of fish oil with higher contents of n-3 polyunsaturated fatty acid (LCPUFA). The contemporaneous vitamin B(6)deficiency and presence of fish oil caused a C18:2 increase, a C20:4 decrease, and replacement of some n-6 LCPUFA with n-3 LCPUFA, without changes in the unsaturation index. In liver, TBARS production did not show any differences between dietary conditions, whereas the activities of glutathione-dependent enzymes were stimulated. In heart, fish oil increased lipid peroxidation, especially in the vitamin B(6)-deficient group.

Evaluation of the effect of rifaximin in colon diverticular disease by means of lactulose hydrogen breath test.

To understand better the mechanism by which rifaximin produces symptomatic relief in diverticular disease of the colon, the effect of this antibiotic on orocaecal transit time and on the production of hydrogen by intestinal microflora after ingestion of lactulose was studied in 33 patients with this disease and in 11 healthy subjects. An hydrogen breath test was carried out to measure pulmonary hydrogen excreted during the 3 hours after ingestion of 10 g lactulose. In patients, the hydrogen breath test with lactulose was repeated after treatment with 400 mg rifaximin twice daily for 10 days. In patients under basal conditions and controls, orocaecal transit time did not differ significantly, but hydrogen production was significantly higher in the former (p < 0.02). In patients, transit time and hydrogen excretion in response to lactulose administration did not differ significantly before and after treatment with rifaximin, and these two parameters were inversely correlated both before (r = 0.49, p < 0.01) and after rifaximin (r = 0.58, p < 0.001). Fifteen of the 33 patients showed accelerated transit time after treatment with the antibiotic, 10 showed no variation, and 8 showed prolonged transit. In 19 patients a reduction in hydrogen production was noted after rifaximin, while in 14 an increase was demonstrated. Twenty-one of the 33 patients reported an improvement in their symptoms with rifaximin; of these, only 10 showed accelerated transit time and 9 a reduction in hydrogen production after rifaximin.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of dietary n-3 polyunsaturated fatty acids on plasma lipemic effect of vitamin B6 deficiency.

Since many connections exist between vitamin B6 and lipid metabolism, we aim to investigate the lipemic effect of different dietary intakes of polyunsaturated fatty acids in rats fed a vitamin B6 deficient diet. Diets were either vitamin B6 deficient (-B6) or vitamin B6 sufficient, pair-fed to the deficient group (PF) and ad libitum (N). The diets were combined with normal lipid (LC: soya bean-coconut-palm oils) and fish oil (FO: soya bean-fish oil). The fish oil diet with sufficient vitamin B6 content caused an increase in n-3 long chain polyunsaturated fatty acids and a decrease in arachidonic acid. In the -B6 group fed a normal lipid diet, the arachidonic acid percentage decreased and the linoleic acid percentage increased; in the -B6 group fed fish oil these changes in fatty acid composition, already consequent upon dietary intake of n-3 long chain polyunsaturated fatty acids, did not show further variations. In the dietary condition of vitamin B6 deficiency, plasma cholesterol content increased in rats fed a lipid control diet, whereas no hypocholesterolemic effect was observed in those fed a fish oil diet. Plasma triglyceride contents were not influenced by dietary lipid quality because, in all conditions, the lower food intake of the PF groups caused a decrease and vitamin B6 deficiency caused an elevation in triglyceride contents which reached those of the ad libitum groups. The study highlights the interaction between vitamin B6 and polyunsaturated fatty acids and the opportunity of dietary intake of fish oil to counterbalance some effects of vitamin B6 deficiency.

Interaction among dietary vitamin B6, proteins and lipids: effects on liver lipids in rats.

Vitamin B6 is involved in protein and lipid metabolism. Yet the effect of pyridoxine deficiency has been studied in relation to separate dietary parameters, we aim to investigate the effect of pyridoxine deficiency associated with a high intake of proteins and/or low EFA content in the diet. Vitamin B6 and PLP contents, fatty acid compositions of lipids and phospholipids were determined in liver of groups of rats fed on diets with different amounts of proteins (20-40%) and EFA (2-35%). The results show a complex interaction among tested nutritional factors with a prevailing influence of dietary proteins on lipid content of liver and of low EFA intake and vitamin B6 on PUFA metabolism. The effects of pyridoxine deficiency on lipid metabolism were dependent on the EFA content of the diet.

Real-time PCR and enzyme-linked fluorescent assay methods for detecting Shiga-toxin-producing Escherichia coli in mincemeat samples.

This work aimed to compare real-time polymerase chain reaction (PCR) with the commercially available enzyme-linked fluorescent assay (ELFA) VIDAS ECOLI O157 for detecting Escherichia coli O157 in mincemeat. In addition, a PCR-based survey on Shiga-toxin-producing E. coli (STEC) in mincemeat collected in Italy is presented. Real-time PCR assays targeting the stx genes and a specific STEC O157 sequence (SILO157, a small inserted locus of STEC O157) were tested for their sensitivity on spiked mincemeat samples. After overnight enrichment, the presence of STEC cells could be clearly determined in the 25 g samples containing 10 bacterial cells, while the addition of five bacteria provided equivocal PCR results with Ct values very close to or above the threshold of 40. The PCR tests proved to be more sensitive than the ELFA-VIDAS ECOLI O157, whose detection level started from 50 bacterial cells/25 g of mincemeat. The occurrence of STEC in 106 mincemeat (bovine, veal) samples collected from September to November 2004 at five different points of sale in Italy (one point of sale in Arezzo, Tuscany, central Italy, two in Mantova, Lombardy, Northern Italy, and two in Bologna, Emilia-Romagna, upper-central Italy) was less than 1%. Contamination by the main STEC O-serogroups representing a major public health concern, including O26, O91, O111, O145, and O157, was not detected. This survey indicates that STEC present in these samples are probably not associated with pathogenesis in humans.

Serum pancreatic enzyme assays in acute abdomen: a comparative prospective study.

Serum amylase, pancreatic isoamylase, lipase, trypsinogen and elastase-1 were measured in 100 consecutive patients who were emergency admissions to a surgical department, and in 27 selected patients with proven acute pancreatitis who served as controls. The final diagnoses in the 100 patients of the study group were: acute pancreatitis in eight patients, other digestive diseases in 87, and urogenital tract diseases in five. In the control group, pancreas-specific enzymes were abnormally high in all patients and amylase in 26 out of 27. In the study group, all enzymes were markedly high in all eight patients with acute pancreatitis. In the remaining 92 patients, serum amylase was abnormally high in seven, and at least one pancreatic enzyme was elevated in 16. These elevations were generally mild. The diagnostic efficiency, i.e., the percentage of patients correctly classified, was 96% for pancreatic isoamylase and lipase, 93% for amylase, 91% for elastase-1, and 84% for trypsinogen. We conclude that serum lipase turbidimetric assay is the most suitable test for emergency diagnosis of acute pancreatitis, because it is highly sensitive and specific and simply and quickly performed.

Vitamin B6 deficiency affects antioxidant defences in rat liver and heart.

We have evaluated 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.