Zinc sulphate administered by transdermal iontophoresis improves breaking strength of surgical wounds in skin of alloxan-induced diabetic rats

PURPOSE:To investigate the effect of zinc sulphate administered by transdermal iontophoresis (TDI) on mechanical resistance of surgical wounds performed in the skin of diabetic rats. METHODS:One hundred and sixty male Wistar rats weighing approximately 250g were submitted to an incision surgery at the anterior region of abdomen and randomly distributed into four experimental groups with 40 non-diabetic control animals (G1) and 40 untreated diabetic animals (G2), both without any treatment of incisions; 40 non-diabetic animals (G3) and 40 untreated diabetic animals (G4), both with incisions treated with zinc sulphate, administered for a period of four consecutive days after surgery, in sessions of ten minutes duration, using a continuous-current electrostimulator (Zn + TDI). Each experimental group was further divided into four subgroups with ten rats each to be evaluated on the 4th, 7th, 14th, and 21st day after surgery. In each period were analyzed clinical and laboratory from the animals, and measured the breaking strength and hydroxyproline content (OH-P) of the skin scars. RESULTS: Breaking strength (BS) was significantly reduced (p<0.05) in skin scars of untreated diabetic rats (G2) on the 7th, 14th, and 21st postoperative days when compared to non-diabetic control rats (G1). In contrast, BS in skin scars of non-diabetic and untreated diabetic rats (G3, G4) treated with Zn + TDI showed significant increase (p<0.05) in those periods when compared with their respective controls with untreated incisions. The OH-P content of the scars did not show statistically significant variation in all studied groups at four different times evaluated after surgery. CONCLUSIONS: Zinc sulphate administered by transdermal iontophoresis had beneficial effect on the mechanical resistance of scars produced in the skin of diabetic rats. This therapeutic may have potential to reduce the complications observed in surgical wounds of the skin in diabetic subjects, mainly in most vulnerable stages of incisions to dehiscences, leakages and infections.

Diabetes mellitus triggers oxidative stress in the liver of alloxan-treated rats: a mechanism for diabetic chronic liver disease

PURPOSE: To investigate whether Diabetes mellitus chemically induced by alloxan is capable of changing, in the long term, the oxidative balance in the liver tissue of rats. METHODS: Sixty male Wistar rats, weighing 250-280g, were randomly distributed into two experimental groups: NG - 30 non-diabetic control rats; DG - 30 alloxan- induced diabetic rats without any treatment for the disease. Each group was further divided into three subgroups containing ten rats each, which were sacrificed after one, three and six months of follow-up, respectively. Blood glucose, urinary glucose, glycosylated hemoglobin and insulin were determined in the plasma of all animals at the beginning of the experiment and prior to all sacrifice periods. The concentrations of lipid hydroperoxides (HP) and the activity of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were also measured in the liver tissue of all animals. RESULTS: Rats from the DG group showed high levels of blood glucose, urinary glucose, and glycosylated hemoglobin, with significantly lower plasma insulin levels than those observed in NG rats (p<0.001). Diabetic animals also showed increased concentration of HP free radicals in the liver tissue as compared to those shown by NG animals after one, three and six months of follow-up. In contrast, the antioxidant activity of the enzymes SOD, CAT and GSH-Px was significantly reduced in all follow-up periods (p<0.01). CONCLUSIONS: Diabetes determines oxidative stress in the liver, which is characterized by increased concentration of reactive oxygen species (ROS) in tissue and significant reduction in their antioxidant defenses. Such oxidative unbalance in the liver cells may play a relevant role in the genesis of the diabetic chronic liver disease, including the non-alcoholic fatty liver disease and its occasional progression to steatohepatitis and cirrhosis.