Reference range for micronutrients and nutritional marker proteins in cord blood of neonates appropriated for gestational ages.

BACKGROUND: Reference values of numerous micronutrients at different gestational ages (GA) have not been yet reported based on large series. AIMS: This study aimed to establish the reference range for zinc, copper, selenium, vitamin A, vitamin E, retinol binding protein, transthyretin, albumin, transferrin and ceruloplasmin in neonates and to give the profiles according to gestational age. STUDY DESIGN: A total of 510 infants appropriate for gestational age were included in the study. The determinations were done using the serum cord blood of 262 term and 248 preterm infants (gestational age of 37 to 42 and 26 to 36 weeks, respectively). RESULTS: All nutrients correlated significantly with birth weight and gestational age but different patterns were highlighted. Vitamin A, retinol binding protein and prealbumin showed a triphasic pattern with a cut-off at about 36 to 39 weeks. In this period, these parameters rised significantly (P<0.001). Albumin and selenium showed a biphasic pattern with a significant positive correlation (P<0.001) between weeks 26 to 38. Transferrin and ceruloplasmin associated with copper showed a continuous increase with GA (P<0.001). On the opposite, zinc and vitamin E decreased. Zinc showed a biphasic pattern with a significant negative correlation (P<0.001) between the 26th to 34th weeks. Vitamin E presented a triphasic pattern with a cut-off at about 32 to 35 weeks (P<0.001). CONCLUSION: The large number of data allow the build-up of reference ranges and charts for the evaluation of micronutrients and proteins in high-risk neonates.

Effect of subacute oral doses of nivalenol on immune and metabolic defence systems in mice.

Nivalenol (NIV) is a toxic Fusarium secondary trichothecene metabolite occurring naturally in cereal grains. In order to evaluate the no observed adverse effect level (NOAEL), we tested the effects of a large array of oral doses of this toxin for responses on plasma biochemistry, the immune system and hepatic drug metabolism in mice. C57Bl6 mice received oral doses of toxin (0.014, 0.071, 0.355, 1.774 or 8.87 mg/kg bw) 3 days a week for 4 weeks. Only the highest dose of NIV induced an increase in plasma phosphate, decreases in plasma urea and immunoglobulin M and additional changes like increases in plasma alkaline phosphatase and immunoglobulin G. Interleukin 4 production was increased in cultured murine splenocytes. Regarding liver drug metabolising enzymes, the only glutathione transferase activity accepting 1-chloro-2,4-dinitro-benzene as substrate was transiently increased in mice receiving low doses (0.071 and 0.355 mg/kg bw) of NIV. Regarding the cytochrome P450 monooxygenases, no significant change was observed in ethoxyresorufin O-deethylase activity whereas both methoxyresorufin and pentoxyresorufin O-dealkylase activities were decreased by 38-45% for the highest dose (8.87 mg/kg bw) of NIV. However, when analysed by Western blot analysis, the protein expression of mouse P450 1a, 2b, 2c, 3a and 4a subfamilies was unchanged in animals receiving NIV. In conclusion, the NOAEL of this toxin in our study was 1.774 mg/kg bw, corresponding to an exposure to 5 ppm contaminated food. Indeed hepatotoxicity appears in the only mice treated with a five fold higher oral dose of 8.87 mg/kg bw of NIV. Such exposure levels appear to be by far higher than the maximal natural occurrence measured in European cereals, known to range from 0.34 to 1.86 ppm.

Adipose tissue proadipogenic redox changes in obesity.

The role of inflammation and oxidative stress in the development of obesity and associated metabolic disorders is under debate. We investigated the redox metabolism in a non-diabetic obesity model, i.e. 11-week-old obese Zucker rats. Antioxidant enzyme activities, lipophilic antioxidant (alpha-tocopherol, coenzymes Q) and hydrophilic antioxidant (glutathione, vitamin C) contents and their redox state (% oxidized form), were studied in inguinal white fat and compared with blood and liver. The adipose tissues of obese animals showed a specific higher content of hydrophilic molecules in a lower redox state than those of lean animals, which were associated with lower lipophilic molecule content and lipid peroxidation. Conversely and as expected, glutathione content decreased and its redox state increased in adipose tissues of rats subjected to lipopolysaccharide-induced systemic oxidative stress. In these in vivo models, oxidative stress and obesity thus had opposite effects on adipose tissue redox state. Moreover, the increase in glutathione content and the decrease of its redox state by antioxidant treatment promoted in vitro the accumulation of triglycerides in preadipocytes. Taken together and contrary to the emergent view, our results suggest that obesity is associated with an intracellular reduced redox state that promotes on its own the development of a deleterious proadipogenic process.