Anthropometric evaluation and micronutrients intake in patients submitted to laparoscopic Roux-en-Y gastric bypass with a postoperative period of ≥1 year

Backgroung - Bariatric surgery is indicated as the most effective treatment for morbid obesity; the Roux-en-Y gastric bypass (RYGB) is considered the procedure of choice. However, nutritional deficiency may occur in the postoperative period as a result of reduced gastric capacity and change in nutrients absorption in the gastrointestinal tract. The prescription of vitamin and mineral supplementation is a common practice after RYGB; however, it may not be sufficient to prevent micronutrient deficiencies. The aim of this study was to quantify the micronutrient intake in patients undergoing RYGB and verify if the intake of supplementation would be enough to prevent nutritional deficiencies. Methods - The study was conducted on 60 patients submitted to RYGB. Anthropometric, analytical, and nutritional intake data were assessed preoperatively and 1 and 2 years postoperatively. The dietary intake was assessed using 24-h food recall; the values of micronutrients evaluated (vitamin B12, folic acid, iron, and calcium) were compared to the dietary reference intakes (DRI). Results - There were significant differences (p < 0.05) between excess weight loss at the first and second year (69.9 ± 15.3 vs 9.6 ± 62.9 %). In the first and second year after surgery, 93.3 and 94.1 % of the patients, respectively, took the supplements as prescribed. Micronutrient deficiencies were detected in the three evaluation periods. At the first year, there was a significant reduction (p < 0.05) of B12, folic acid, and iron intake. Conclusions - Despite taking vitamin and mineral supplementation, micronutrient deficiencies are common after RYGB. In the second year after surgery, micronutrient intake remains below the DRI

Toxicity of zinc oxide to scleractinian corals and zooxanthellae: a brief review

In recent years, the safety of sunscreens to coral reefs and the role these products would play in the process of coral bleaching has been a concern. However, the discussion centers almost exclusively on the organic components used as UV filters, with little attention given to inorganic UV filters, such as zinc oxide. Zinc oxide nanoparticles (ZnO-NPs) have been a common ingredient of sunscreen formulations for decades and are being discharged in coral reef environments. Even though there are data supporting that ZnO is toxic to certain species of fish and algae, regulatory agencies do not appear concerned with the possible outcome of the exposure of corals and their algal symbionts to this metal oxide. This review compiles the published work on the toxicity of ZnO and ZnO-NPs to corals and zooxanthellae, which strongly supports the notion that zinc oxide is toxic to both corals and microalgae. In view of this, concern has been raised by the use of the “reef safe” label to promote sunscreens that lack specific organic components, however containing ZnO as the major UV filter

Effects of human serun albumin in some biological properties of rhodium(II) complexes

The affinities for human albumin (HSA) of five rhodium(II) complexes of general formula [Rh2(bridge)4] (bridge = acetate, propionate, butyrate, trifluoroacetate and trifluoroacetamidate) were determined by spectrophotometry. In the case of the alkylcarboxylates, an inverse correlation of affinity with their liposolubilities was observed. Diffusion of the free or protein-bound complexes into Ehrlich cells in vitro seems to be primarily governed by the hydrophobic character of the complex. The complex [Rh2(tfc)4] exhibited affinity towards the protein (K = 214.1) as well as cell partition both in the absence (32.1%) and presence (48.6%) of HSA. The compound HSA: [Rh2(tfc)4] has had its antitumoral action in tumor-bearing Balb-c mice investigated, showing that HSA can be a drug reservoir for the rhodium complex

Mitochondria-penetrating peptides conjugated to desferrioxamine as chelators for mitochondrial labile iron

<div><p>Desferrioxamine (DFO) is a bacterial siderophore with a high affinity for iron, but low cell penetration. As part of our ongoing project focused on DFO-conjugates, we synthesized, purified, characterized and studied new mtDFOs (DFO conjugated to the Mitochondria Penetrating Peptides TAT_49-57, 1A, SS02 and SS20) using a succinic linker. These new conjugates retained their strong iron binding ability and antioxidant capacity. They were relatively non toxic to A2780 cells (IC50 40–100 μM) and had good mitochondrial localization (Rr +0.45 –+0.68) as observed when labeled with carboxy-tetramethylrhodamine (TAMRA) In general, mtDFO caused only modest levels of mitochondrial DNA (mtDNA) damage. DFO-SS02 retained the antioxidant ability of the parent peptide, shown by the inhibition of mitochondrial superoxide formation. None of the compounds displayed cell cycle arrest or enhanced apoptosis. Taken together, these results indicate that mtDFO could be promising compounds for amelioration of the disease symptoms of iron overload in mitochondria.</p></div

IC₅₀ (μM) of mtDFO, DFO and TAMRA-tagged mtDFO in A2780 cells after 24 h.

<p>IC₅₀ (μM) of mtDFO, DFO and TAMRA-tagged mtDFO in A2780 cells after 24 h.</p

Structures of DFO and mtDFO in this study.

<p>The succinyl linker is grayed. Dmt: 2’,6’-dimethyltyrosine; F_X: cyclohexylalanine; r: <i>d</i>-arginine.</p