Effects of desipramine on the antioxidant status in rat tissues at carrageenan‐induced paw inflammation

The pathogenesis of many diseases and different pathological conditions, including inflammation, is associated with excess production of reactive oxygen species (ROS). The present study aimed to investigate the effects of the antidepressant desipramine (DES) on carrageenan (CG)‐induced inflammation, as well as on the endogenous levels of cell enzyme and non‐enzyme antioxidants in rat liver and spleen, 4 and 24 h after CG injection. The intra‐plantar CG injection into the right hind paw resulted in a time‐dependent increase in the paw volume; the maximum of CG‐induced edema peak was in 2–4 h. A single DES dose of 20 mg·kg^?1, administered 30 min before CG, had no effect on paw edema, whereas the higher drug dose used (50 mg·kg^?1) suppressed the edematous response to CG. The latter drug dose protected CG‐induced decrease of glutathione (non‐enzyme antioxidant) in the liver; it did not affect CG‐unchanged activities of superoxide dismutase, glutathione peroxidase (enzyme antioxidants) and glucose‐6‐phosphate dehydrogenase (enzyme, important for the activity of glutathione‐conjugated antioxidant enzymes) in both liver and spleen. The drug showed an efficient antioxidant capacity in ROS‐generating chemical systems; it was higher than that of fluoxetine (another type of antidepressant). The present results suggest that the good antioxidant activity of DES might contribute to its beneficial effects in liver injuries. Copyright © 2011 John Wiley & Sons, Ltd.     

Detection of small RB1 gene deletions in retinoblastoma by multiplex PCR and high-resolution gel electrophoresis

Summary Loss of function of both copies of the RB1 gene is a causal event in the development of retinoblastoma. The predisposition to this tumor can be inherited as an autosomal dominant trait. Direct detection of the genetic defect is important for presymptomatic DNA diagnosis and genetic counseling in families with hereditary retinoblastoma. We have used multiplex polymerase chain reaction and high-resolution polyacrylamide gel electrophoresis to detect RB1 gene deletions as small as one base pair. By using three independent sets of amplification reactions, which cover 26% of the RB1 gene coding region, we identified RB1 gene deletions in the DNA of peripheral blood cells in 3 out of 24 (12.5%) unrelated patients with hereditary retinoblastoma. In one case, formalin-fixed paraffin-embedded tumor material was also used to detect the mutation. Sequencing of the mutated alleles revealed deletions of 1, 3 and 10 base pairs. Each deleted region was flanked by direct repeats.     

The use of tucumã oil (<Emphasis Type="Italic">Astrocaryum vulgare</Emphasis>) in alloxan-induced diabetic mice: effects on behavior,oxidant/antioxidant status,and enzymes involved in brain neurotransmission

Diabetes increases the risk of vascular events and mortality. While earlier type 2 diabetes trials demonstrated that intensive glucose lowering reduces microvascular complications, it is only recently that treatment with some of the newer antihyperglycemic agents has been associated with macrovascular benefits. We report herein that db/db mice concomitantly fed the Western diet and treated with the anti-inflammatory agent methotrexate display a less aggressive inflammatory (lower serum IL-1β, IL-6, SDF-1, and TNFα levels; higher circulating adiponectin, IL-12p70 and IL-10 concentrations; lower aortic VCAM-1 levels) profile than their saline-treated counterpart. Furthermore, acetylcholine-elicited endothelium-dependent vasodilatation was significantly greater in thoracic aortic segments from the former group. Collectively, the data lend support to the notion that alterations in the inflammatory system may be involved in the macrovascular benefits observed in type 2 diabetes trials and provide credence for the development of anti-inflammatory tools to lower CV risk and CV events in diabetes.     

Duck skeletal muscle acylphosphatase: Primary structure

The complete amino acid sequence of duck skeletal muscle acylphosphatase is presented. The sequence was studied by the manual Edman degradation of the complete series of tryptic peptides and the amino acid composition of peptic peptides. The NH₂-terminus is acetylated, and the polypeptide consists of 102 amino acid residues. The sequence is compared with other known acylphosphatases from the skeletal muscle of several vertebrate species.     

Effects of ultraviolet radiation on human cutaneous nerve fibres

Due to an increasing number of skin diseases as a result of exposure to ultraviolet (UV) radiation, it is necessary to evaluate the effectiveness of new skin care formulations with broad-spectrum sunscreens.
Objectives:  This study aims to assess the status of nerve fibres in healthy human skin, to quantify effects of UV radiation on nerve endings, and to evaluate neuroprotective effects of new skin care formulations against UV exposure damage.
Methods:  Samples were obtained from 34 female patients enrolled for plastic surgery and were immediately treated (10 min) with three emulsions: Cream 1, Cream 2 (placebo) and a sunscreen with sun protection factor 15 (SPF15). Control samples and those treated with the cream emulsions were exposed to UVA and UVB for 60 min. Nerve fibres were identified by immunofluorescence using a monoclonal antibody (anti-human CD56/NCAM). Cell damage was assessed by image analysis.
Results:  Several cellular nervous structures were identified in the skin samples, including free nerve endings. UVA and UVB significantly decreased (40–60%) density of nerve endings in the control samples and those treated with placebo (Cream 2) or SPF15 (all P  < 0.001). Cream 1 completely blocked effects of UV radiation on nerve endings ( P  > 0.05 vs. control).
Conclusions:  Quantification of cell damage induced by UV radiation provides useful information for identification of new skin care compounds with neuroprotective properties.     

Progressive loss of cytochrome c oxidase in the human extraocular muscles in ageing--a cytochemical-immunohistochemical study.

Cytochrome c oxidase (complex IV of the respiratory chain) was studied histochemically in autoptic human extraocular muscles (n = 135), revealing randomly distributed single fibers without enzyme activity. The enzyme defect was expressed in all the mitochondria of an involved fiber as evidenced by ultracytochemistry. Succinate dehydrogenase showed normal histochemical reactivity. The defects occurred already in the second decade and were regularly seen from the third decade on. The defect density (defects/mm2) increased from approx. 1/mm2 below the fifth decade to about 4/mm2 in advanced age (P = 0.000). The highest defect density was observed in the levator palpebrae muscle. On the whole, the defect density was about 5-6 times higher in the extraocular muscles than in the limb muscle, diaphragm and heart (Müller-H?cker, 1989, 1990). Immunocytochemical detection of cytochrome c oxidase showed that loss of cytochrome c oxidase activity was due to an almost complete absence of both nuclear and mitochondria subunits of the enzyme. The results document different organ and heterogenic cellular sensitivity to the age-related loss of cytochrome c oxidase. The loss of both mitochondrial and nuclear subunits indicates that nuclear factors are most probably involved in the decline of the respiratory chain function in senescence.