Maternal/neonatal vitamin D deficiency: a risk factor for bronchopulmonary dysplasia in preterms?

OBJECTIVE: The objective of this study was to investigate the possible association between maternal/neonatal 25-hydroxy vitamin D (25-OHD) levels and development of bronchopulmonary dysplasia. STUDY DESIGN: One hundred and thirty-two preterm infants ⩽32 weeks of gestation who were diagnosed with respiratory distress syndrome were enrolled. 25-OHD levels were determined in maternal/neonatal blood samples that were obtained at the time of admission to the neonatal intensive care unit. RESULT: A total of 100 infants were included and 31 (31%) developed bronchopulmonary dysplasia (BPD). Both maternal and neonatal 25-OHD levels in the BPD group were significantly lower compared with those in the no-BPD group (P=0.0001). A positive correlation was detected between maternal and neonatal 25-OHD levels. All of the infants with BPD had a 25-OHD level <10 ng ml(-1), which represented severe deficiency. Univariate logistic regression analysis revealed that maternal/neonatal vitamin D levels were a significant predictor of BPD (odds ratio (OR): 0.76 and 0.61, respectively, P<0.001). CONCLUSION: We demonstrated for the first time that lower maternal and neonatal vitamin 25-OHD levels were associated with BPD development in preterm infants. However, further studies with larger sample sizes are needed to delineate the possible link between vitamin D deficiency and BPD.

Lower vitamin D levels are associated with increased risk of early-onset neonatal sepsis in term infants.

OBJECTIVE: To evaluate the effect of vitamin D levels on early-onset sepsis (EOS) in term infants. STUDY DESIGN: Fifty term infants with clinical and laboratory findings of EOS (study group) and 50 healthy infants with no signs of clinical/laboratory infection (control group) were enrolled. Blood was drawn at the time of admission during the first 3 postnatal days of life in both groups for measurement of 25-hydroxyvitamin D (25-OHD) levels. RESULT: Maternal and neonatal 25-OHD levels (22.2/8.6 ng ml(-1), respectively) in the study group were significantly lower than those of the control group (36.2/19 ng ml(-1), respectively, P<0.001). A positive correlation was detected between maternal and neonatal 25-OHD levels. Severe vitamin D deficiency was significantly more common in the sepsis group. CONCLUSION: Lower maternal and neonatal 25-OHD levels are associated with EOS. These data suggest that adequate vitamin D supplementation during pregnancy may be helpful to prevent EOS in term neonates.

The relation between oxidative stress, inflammation, and neopterin in the paraquat-induced lung toxicity.

Paraquat (PQ) is a well-known quaternary nitrogen herbicide. The major target organ in PQ poisoning is the lung. Reactive oxygen species (ROS) and inflammation play a crucial role in the development of PQ-induced pulmonary injury. Neopterin is synthesized in macrophage by interferon γ and other cytokines. We aimed to evaluate the utility of neopterin as a diagnostic marker in PQ-induced lung toxicity. Sprague Dawley rats were randomly divided into two groups (sham and PQ), administered intraperitoneally 1 mL saline and PQ (15 mg/kg/mL) respectively. Blood samples and lungs were collected for analyses. Lung injury and fibrosis were seen in the PQ group. Serum total antioxidant capacity, lactate dehydrogenase (LDH), and lung transforming growth factor-1ß (TGF-1ß) levels were significantly higher than the sham group (in all, p < 0.001). In addition, in the PQ group, serum neopterin and lung malondialdehyde (MDA) levels were also significantly higher than the sham group (in all, p = 0.001). Serum neopterin levels were correlated with LDH activities, lung MDA, lung TGF-1ß levels, and the degree of lung injury. These findings demonstrated that oxidative stress, reduction of antioxidant capacity, and inflammation play a crucial role in the PQ-induced lung injury. Elevated serum neopterin levels may be a prognostic parameter to determine extends of PQ-induced lung toxicity. Further studies may be performed to clarify the role of neopterin by different doses of PQ.

Aspartame induces angiogenesis in vitro and in vivo models.

Angiogenesis is the process of generating new blood vessels from preexisting vessels and is considered essential in many pathological conditions. The purpose of the present study is to evaluate the effect of aspartame on angiogenesis in vivo chick chorioallantoic membrane (CAM) and wound-healing models as well as in vitro 2,3-bis-2H-tetrazolium-5-carboxanilide (XTT) and tube formation assays. In CAM assay, aspartame increased angiogenesis in a concentration-dependent manner. Compared with the control group, aspartame has significantly increased vessel proliferation (p < 0.001). In addition, in vivo rat model of skin wound-healing study showed that aspartame group had better healing than control group, and this was statistically significant at p < 0.05. There was a slight proliferative effect of aspartame on human umbilical vein endothelial cells on XTT assay in vitro, but it was not statistically significant; and there was no antiangiogenic effect of aspartame on tube formation assay in vitro. These results provide evidence that aspartame induces angiogenesis in vitro and in vivo; so regular use may have undesirable effect on susceptible cases.

Hyperbaric oxygen treatment and N-acetylcysteine ameliorate acetaminophen-induced liver injury in a rat model.

An overdose of acetaminophen (APAP) produces centrilobular hepatocellular necrosis. We aimed to investigate the hepatoprotective effects of N-acetylcysteine (NAC) only and hyperbaric oxygen (O(2)) treatment (HBOT) combined with NAC, and their anti-inflammatory properties in liver tissue. In the current study, a total of 32 male Sprague Dawley rats were divided into 4 groups: sham, APAP, NAC, and NAC + HBOT. In the APAP, NAC, and NAC + HBOT groups, liver injury was induced by oral administration of 1 g/kg APAP. The NAC group received 100 mg/kg NAC per day. NAC + HBOT group received intraperitoneal injection of 100 mg/kg/day NAC and were given HBOT at 2.8 ATA pressure with 100% O(2) inhalation for 90 min every 12 h for 5 days. Rats in the sham group received distilled water only by gastric tube. All animals were killed on day 6 after APAP or distilled water administration. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, hepatic neopterin, tumor necrosis factor-α (TNF-α), and interleukin 6 (IL-6) levels were measured. There was a significant increase in serum AST and ALT activities in the APAP group compared with the sham group (in both p = 0.001). NAC and NAC + HBOT groups had significant decreases in hepatic neopterin, TNF-α, and IL-6 levels compared with the APAP group. APAP administration caused extensive hepatic necrosis. NAC and NAC + HBO treatments significantly reduced APAP-induced liver injury. Our results showed that the liver damage in APAP toxicity was attenuated by NAC and NAC + HBO treatments. NAC + HBOT exhibit hepatoprotective activity against APAP-induced liver injury in rats.