Differences in tissue fatty acid composition between reared and wild sharpsnout sea bream, Diplodus puntazzo (Cetti, 1777).

The fatty acid composition and lipid content of white muscle, liver and mesenteric fat, in reared v. wild sharpsnout sea bream (Diplodus puntazzo) were compared. The mesenteric fat index fat weight/body weight) and the lipid contents of both white muscle and liver proved consistently higher in farmed v. wild sharpsnout sea bream (79.0 (SE 13.1) v. 38.7 (SE 5.1) g/kg, 188.4 (SE 30.0) v. 58.2 (SE 3.9) g/kg and 27.2 (SE 3.7) v. 17.3 (SE 1.9) g/kg, respectively). The higher values of linoleic, eicosapentaenoic, docosahexaenoic and n-3 series acids in reared fish muscle make reared sharpsnout more favourable for human consumption. In reared fish mesenteric fat, polyunsaturated fatty acids reached higher levels (32.54 (SE 0.71) g/100 g total fatty acids than those found in wild fish (26.08 (SE 1.38) g/100 g total fatty acids or even present in the diet (28.34 g/100 g total fatty acids). Compared with cultured fish, wild sharpsnout displayed a higher content of n-3 fatty acids in liver fat (31.67 (SE 1.13) g/100 g total fatty acids), but lower in mesenteric fat (20.35 (SE 1.41) g/100 g total fatty acids). Atherogenic index values were similar for wild and reared fish in all tissues, while the index of thrombogenicity of muscle and mesenteric fat (0.353 (SE 0.012) and 0.402 (SE 0.021) respectively) was significantly increased in wild fish probably due to the omnivorous habits of the species and/or to seasonal food variations. Depending on the time of the year or the season, reared fish could be more suitable for human consumption than wild fish.     

Familial benign chronic pemphigus

In connection with three of eight recent cases of familial benign chronic pemphigus (FBCP) a brief review of its clinical, immunofluorescent, microscopic, and ultramicroscopic characteristics was made, with special emphasis on the differential diagnosis. The two main clinical aspects of the disease are emphasized: the moist, macerated, and intertriginous (candidiasis-like) variety, and the polycyclic plaque, with active and lichenoid edges (tinea corporis-like). Treatment was only partially successful, but slightly more effective with the lichenoid form of disease.     

Lung cell toxicity experimentally induced by a mixed dust from Mexicali, Baja California, Mexico.

Lung disease caused by nonoccupational exposures to inorganic particles from the soil has been reported in several areas of the world. We tested the toxic potential of dust samples from a Mexican city (Mexicali) that is frequently affected by dust storms and is geographically related to the area of San Diego, CA, where constituents of the soil have been reported to be fibrogenic. We found that samples of Mexicali dust are a mixture of approximately 75% potassium aluminum silicates (illite) and approximately 20% silica. Respirable size particles were highly hemolytic and induced lactic dehydrogenase release from alveolar macrophages exposed in vitro. Animals instilled intratracheally with the dust developed a multifocal interstitial lung disease associated with deposits of the aluminum silicates, which were identified by X-ray microanalysis. Inhalation studies in rats demonstrated that the majority of particles were deposited preferentially at the first alveolar duct bifurcations. Twenty-four hours later, numerous particles had been ingested by alveolar macrophages that had migrated to those sites of deposition. It is proposed that alveolar macrophages are attracted to the deposited particles by complement fragments since Mexicali dust is capable of activating complement proteins from both serum and bronchoalveolar lavage. Activation resulted in alveolar macrophage chemotaxis. Mexicali dust induced biological activities and lung changes similar to those of asbestos and silica, suggesting that this material could be an etiologic agent of pulmonary fibrosis in exposed individuals.     

Thinner inhalation effects on oxidative stress and DNA repair in a rat model of abuse

Humans can come into contact with thinner by occupational exposure or by intentional inhalation abuse. Numerous studies of workers for genotoxic effects of thinner exposure have yielded conflicting results, perhaps because co‐exposure to variable other compounds cannot be avoided in workplace exposure studies. In contrast, there is no data concerning the genotoxic effects of intentional inhalation abuse. The aim of this project was to examine the genotoxic effects of thinner inhalation in an animal model of thinner abuse (rats exposed to 3000 ppm toluene, a high solvent concentration over a very short, 15 min time period, twice a day for 6 weeks). The data presented here provides evidence that thinner inhalation in our experimental conditions is able to induce weight loss, lung abnormalities and oxidative stress. This oxidative stress induces oxidative DNA damage that is not a characteristic feature of genotoxic damage. No significant difference in DNA damage and DNA repair (biomarkers of genotoxicity) in lymphocytes from thinner‐treated and control rats was found. Lead treatment was used as a positive control in these assays. Finally, bone marrow was evaluated as a biomarker of cellular alteration associated with thinner inhalation. The observed absence of hemopoietic and genetic toxicity could be explained in part by the absence of benzene, the only carcinogenic component of thinner; however, benzene is no longer a common component of thinner. In conclusion, thinner did not cause genotoxic effects in an experimental model of intentional abuse despite the fact that thinner inhalation induces oxidative stress. Copyright © 2009 John Wiley & Sons, Ltd.