l-carnitine and cancer cachexia: Clinical and experimental aspects

Cancer cachexia is a multifaceted syndrome characterized, among many symptoms, by extensive muscle wasting. Chronic systemic inflammation, partly triggered and sustained by cytokines, as well as increased oxidative stress contributes to the pathogenesis of this complex metabolic disorder. l-carnitine plays a central role in the metabolism of fatty acids and shows important antioxidant and anti-inflammatory properties. Systemic carnitine depletion has been described in several diseases, and it is characterized by fatigue, muscle weakness, and decreased tolerance to metabolic stress. In cachectic cancer patients, low serum carnitine levels have been reported, and this change has been suggested to play an important contributory role in the development of cachexia. Based on these data, carnitine supplementation has been tested in preliminary studies concerning human cachexia, resulting in improved fatigue and quality of life. We present here a review of clinical and experimental evidence regarding the use of carnitine supplementation in the management of cancer cachexia

The Role of Cholecystokinin in the Gastroprotective Effect of Apelin Against to Ischemia/Reperfusion-Induced Injury

WOS: 000453220100032…Akdeniz UniversityAkdeniz University [TDK-2015-593]Akdeniz University, Scientific Research Project No: TDK-2015-593

Cadmium-induced changes in parietal cell structure and functions of rats

PubMedID: 11051589The aim of this study was to determine the cadmium (Cd)-induced functional and structural changes in gastric parietal cells of male rats exposed to high Cd for 30 d. In the present study, control animals were fed with normal food and tap water; the remaining animals received Cd (15 ppm CdCl2) in drinking water for the same period. Receiving Cd for 30 d increased the mean blood Cd level, the mean tissue Cd content, and the mean blood pressure (p < 0.01, p < 0.001, p < 0.01, respectively). The basal acid output fell; however, the increases in stimulated acid output were not statistically significant. Light and electron microscopic examination revealed respectively that (1) Cd decreases the mean parietal cell number per unit from the control value of 23.46 ± 3.84 to 19.46 ± 2.12 (p < 0.05) and it affected preferentially the cells located at the distal half of the zymogenic unit and (2) in parietal cells, the Cd-induced alterations were characterized with swollen canalicular profiles, broken-down tubulovesicles, or degenerated mitochondria. We concluded that Cd augments the elimination rate of parietal cells by increasing the alteration rate and reduced basal acid output can be explained easily with the loss of parietal cell population.This work was supported by the Research Fund of Akdeniz University, Antalya, Turkey, (grant no: 95. 03. 0103. 06)

Effect of sulfite on macrophage functions of normal and sulfite oxidase-deficient rats

Sulfite has both an endogenous and an exogenous provenance in the mammalian tissues. The aim of the present study was to assess the effect of sulfite on macrophages functions in normal or sulfite oxidase deficient rats. Rats were divided into eight groups; (1) control group, (2) sulfite group (the rats received sodium meta bi-sulfite (25 mg/kg) in drinking water for 6 weeks), (3) vitamin E group (the rats received Vit E (50 mg/kg) by gavage for 6 weeks), (4) sulfite group + Vit E, (5)sulfite oxidase deficient group (the rats received high-W/Mo-deficient diet. The activity of sulfite oxidase was reduced in rats maintained on the high-W/Mo-deficient diet during the first 21 days of treatment. After the sulfite-oxidase deficiency, the rats continued to receive high-W/Mo-deficient diet for 6 weeks.), (6) sulfite + sulfite oxidase deficient group, (7) Vit E + sulfite oxidase deficient group, and (8) sulfite + Vit E + sulfite oxidase deficient group. Sulfite caused a significant increase in phagocytic and chemotactic activities of peritoneal macrophages. In sulfite-oxidase deficient rats, the increase in phagocytic and chemotactic activities in peritoneal macrophages after sulfite intake was found more than the control rats. Vit E supplementation prevented sulfite induced increase in macrophages functions. These results show that the macrophage functions are sensitive to sulfite intake. The effect of sulfite on macrophage functions may be related to reactive oxygen species. Because Vit E administration was able to modulate significantly sulfite-induced changes in the functions of peritoneal macrophages. © 2005 Elsevier Ltd. All rights reserved

Zaštitni učinak dokozaheksaenske kiseline na želudac muških C57BL/6 miševa s Parkinsonovom bolešću izazvanom s MPTP

The purpose of this study was to detect gastric changes in Parkinson’s disease induced by 1-methyl-4-phenyl-1.2.3.6.-tetrahydropyridine (MPTP), and to investigate the protective effect of docosahexaenoic acid (DHA) against these changes in mice. The mice were divided into 4 groups (n=10 in per group) as control, DHA, Parkinson and DHA+Parkinson groups. DHA was administered by gavage for 30 days. On the 23rd day of gavage treatment, the animals of the Parkinson and DHA+Parkinson groups were intraperitoneally injected with MPTP. Seven days after the injection of MPTP, their locomotor activity, bradykinesia and rotarod performance were measured. Tyrosine hydroxylase expression in substantia nigra and the apoptotic index, the concentrations of tumor necrosis factor-α and histamine, and the number of mast cells in the stomach were evaluated. Administration of DHA significantly prevented the reduction in motor functions (P<0.001) and nigral TH neurons (P<0.05), and apoptosis (P<0.05), and an increase in TNF-α concentration (P<0.01) in the stomach. An increase in the number of mast cells in the stomach wall was observed in PD (P<0.001). DHA prevented the increase in the number of mast cells (P<0.05) and the histamine level (P<0.01) due to PD. As a result, MPTP administration in mice caused changes in the stomach as well as impairment in motor functions, and DHA was observed to reduce these changes.U radu je istražen zaštitni učinak dokozaheksaenske kiseline (DHA) na želučane promjene u muških miševa s Parkinsonovom bolešću (PD), izazvanom 1-metil-4-fenil-1.2.3.6.-tetrahidropiridinom (MPTP). C57BL/6 miševi su podijeljeni u četiri skupine (n = 10 po skupini): kontrolnu skupinu, skupinu DHA, skupinu Parkinson i skupinu DHA + Parkinson. DHA je primjenjivana pomoću sonde 30 dana. Dvadeset treći dan životinjama u skupinama Parkinson i DHA + Parkinson intraperitonealno je injiciran MPTP. Sedam dana poslije primjene MPTP-a izmjerena je lokomotorna aktivnost, bradikinezija i proveden rotarod-test. Procijenjeni su ekspresija tirozin-hidroksilaze (TH u substantia nigra), apoptotički indeks, koncentracije faktora tumorske nekroze alfa (TNF-α) i histamina te broj mastocita u želucu. Primjena DHA znakovito je prevenirala smanjenje motoričkih funkcija (P < 0,001) i TH neurona (P < 0,05) te apoptoze (P < 0,05), a povećala koncentraciju TNF-α (P < 0,01) u želucu. Porast broja mastocita u želučanoj stijenci utvrđen je u skupinama s PD (P < 0,001). DHA je prevenirala porast broja mastocita (P < 0,05) i razine histamina (P < 0,01) zahvaljujući PD-u. Zaključeno je da primjena MPTP-a u miševa uzrokuje promjene u želucu i motoričkim funkcijama te da DHA utječe na smanjenje tih promjena