Arginine Silicate Inositol Complex Accelerates Cutaneous Wound Healing

The objective of this study was to assess the accumulation and depletion of cadmium in the blood, milk, hair, feces, and urine of Holstein cows during and after treatment. Three Holstein cows received daily oral cadmium administrations (as cadmium chloride) of 0.182 mg/kg body weight/day for 21 days followed by a 63-day withdrawal period. Blood, milk, hair, feces, and urine were collected during treatment and withdrawal periods. Cadmium concentrations were measured by inductively coupled plasma mass spectrometry (ICP-MS). Cadmium concentrations in blood (0.61–1.12 μg/L), milk (0.39–1.04 μg/L), and urine (0.41–2.05 μg/L) were low. Comparatively, cadmium concentrations in feces were higher, especially on treatment day 14 (20.11 mg/kg dry matter). Fecal cadmium concentrations decreased to baseline levels (0.12 mg/kg dry matter) on withdrawal day 21. Hair cadmium concentrations increased with treatment, reaching the highest levels on withdrawal day 7 (24.33 μg/kg). Most of the cadmium was excreted via the feces and very little was present in urine or milk. Cadmium residues were detected in blood and milk more than 63 days after cadmium withdrawal. Hair cadmium concentrations may reflect exposure to the metal.     

Pharmacological preconditioning with erythropoietin reduces ischemia–reperfusion injury in the small intestine of rats

AimsConsidering the implications that arose from several recent experimental studies using recombinant human erythropoietin in rodents, erythropoietin has been regarded as a pharmacological preconditioning agent. The purpose of the present study was to evaluate whether erythropoietin has a preconditioning effect against ischemia and reperfusion injury in the small intestine of the rat.Main methodsIntestinal ischemia was induced in male Wistar rats by clamping the superior mesenteric artery for 30 min, followed by reperfusion for 180 min. Recombinant human erythropoietin (1000 or 3000 U/kg) or vehicle was administered intraperitoneally 24 h prior to ischemia. After collection of ileal tissue, evaluation of damage was based on measurements of the accumulation of polymorphonuclear neutrophils by technetium-99m-labeled leukocyte uptake, content of malondialdehyde, reduced glutathione, contractile responses to agonists, and an evaluation of histopathological features in intestinal tissue.Key findingsTreatment with erythropoietin 24 h before ischemia significantly reduced the tissue content of malondialdehyde and increased that of reduced glutathione. Pretreatment also significantly suppressed leukocyte infiltration into the postischemic tissue, as evidenced by the lower content of myeloperoxidase and technetium-99m-labeled leukocytes. Physiological and histopathological improvements were also significant with the rHuEpo treatment.SignificanceResults of the present study indicate that rHuEpo is an effective preconditioning agent in ischemic injury of the small intestine. Protection provided by recombinant human erythropoietin is closely related to the inhibition of oxidative stress and leukocyte infiltration, which might be among the possible protective mechanisms of erythropoietin in intestinal ischemia and reperfusion.