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This study examined the dietary effects of Sanacore®GM (SAN) on growth and production, immune-antioxidative status, cytokines, and the resistance of European sea bass to Vibrio alginolyticus infection. Fish (28.5–32.3 g) were fed on 0.0, 1.0, 2.0, 4.0, 6.0, and 8.0 g SAN/kg feed for ten weeks. Following that, fish were intraperitoneally injected with V. alginolyticus, and observed for further ten days. Among different water quality parameters, only unionized ammonia and nitrite values were significantly declined in groups received 4.0–8.0 g SAN/kg feed. Significant increases in fish growth, production, hematological, and immune-antioxidant indices were observed in SAN-fed fish. Compared with the control group, IL-1β and TNF-α genes expressions were down-regulated in groups fed on 4.0–8.0 g SAN/kg feed. After bacterial infection, low fish mortalities (20%–10%) were observed in fish fed with 4.0–8.0 g SAN/feed, respectively. The polynomial fitting curve demonstrates that the optimum SAN level for European sea bass is 5.0 g/kg feed. [ABSTRACT FROM AUTHOR]

Yeast, Saccharomyces cerevisiae, has been utilized as a probiotic in aqua-feeds to promote growth and alleviate the stress in aquatic animals. On the other hand, cadmium (Cd) toxicity causes serious retardation of growth and welfare status of aquatic animals. The present study was conducted to evaluate the protective role of dietary yeast in mitigating the waterborne Cd toxicity effects on the growth, haemato-biochemical, stress biomarkers, and histopathological investigations of gilthead seabream (Sparus aurata L.). In a 3 × 3 factorial design, the acclimated fish (20–24 g) were randomly distributed into nine treatments in triplicates where they were fed on 0.0% (control), 0.5%, and 1.0% of yeast along with exposure to 0.0, 1.0, and 2.0 mg Cd/L for 60 days. All growth parameters and mRNA expressions of IGF-1 and GH genes as well as haematological parameters were markedly increased with the increase of dietary yeast levels; meanwhile these variables were significantly retarded with Cd exposure. Contradictory effects on the above-mentioned variables were observed with Cd toxicity. In contrast, blood cortisol, glucose, total cholesterol, and triglyceride, lactate dehydrogenase, alanine transaminase, aspartate transaminase, alkaline phosphatase, in addition to DNA fragments % were noticeably increased with Cd toxicity especially at the treatment of 2.0 mg Cd/L, while decreasing with increasing dietary yeast levels. Compared with the control fish group, Cd concentrations in the gill, liver, and muscle tissues of gilthead seabream were higher in Cd-exposed treatments, especially at the treatment of 2.0 mg Cd/L. Deposition of Cd in fish liver was higher than that in gill tissues but lowest Cd residue was observed in muscle tissues. No significant changes in Cd residues in fish organs were observed in yeast-fed fish with no Cd exposure. The Cd exposure negatively affected histological status of gill, liver, and kidney tissues of S. aurata; while feeding Cd-exposed fish on yeast diets lowered the Cd residues in fish organs and recovered the adverse effects of Cd toxicity. Hence, this study recommends the addition of bakery yeast (1.0%) to fish diets to improve the performance, overall welfare, and histopathological status of gilthead seabream, S. aurata. [ABSTRACT FROM AUTHOR]

The aim of this research was to test the hypothesis of an improved growth, feed utilization efficiency, and economic efficiency (EE) of broiler chickens reared on different diets supplemented with spirulina (SPA), cinnamon oil (CO) and citric acid (CA). Total of 128 broiler chicken were divided randomly in to 4 group 32 chicks for each, with 4 replicants (8 bird/replicant). Group1 (control) fed diet without any additives. Group2 fed control diet + spirulina (2g/kg feed). Group3 fed control diet + cinnamon oil (1ml/kg feed). Group4 fed control diet + citric acid (5g/kg feed). The result indicated that SPA, CO, and CA has a significant effect at (p<0.05) on growth performance parameters (feed intake (FI), weight gain (WG) and feed conversion ratio (FCR)). SPA recorded the highest FI while CA recorded the lowest value. It was noticed that SPA and CA do better than CO in live weight and weight gain. The best FCR was in CA group (1.61). SPA and CA has considerable effect at (P<0.05) on dressing percent while, CO had no significant effect. CO and CA had a significant impact at (P<0.05) on thymus relative weight. From The Economic point of view CA and SPA in the select doses had improved economic measures and relative economic efficiency (REE) indicating high return and net profit, benefit cost ratio, profitability percent, net profit margin. In contrast CO had no distinct effect on these parameters in the selected dose. Bearing in mind that citric acid had a preference in improving economic efficiency over spirulina. SPA, CO and CA may be used as feed additives for broiler chicken to enhance growth performance, Economically CA and SPA in the selected doses is better to increase return and profitability. Citric acid has the advantage in terms of its presence in the market and its low price compared to spirulina. [ABSTRACT FROM AUTHOR]

In guinea pig antral mucous cells, ACh stimulates the [Ca.sup.2+]-regulated exocytosis, which has a characteristics feature: an initial transient phase followed by a sustained phase. The effects of cGMP on ACh-stimulated exocytosis were studied in guinea pig antral mucous cells using video microscopy. cGMP enhanced the frequency of ACh-stimulated exocytotic events, whereas cGMP alone did not induce any exocytotic events under the ACh-unstimulated condition, cGMP did not stimulate either [Ca.sup.2+] mobilization or cAMP accumulation. The [Ca.sup.2+] dose-response studies demonstrated that cGMP shifted the dose-response curve upward with no shift to the lower concentration. This indicates that cGMP increased maximal responsiveness of the [Ca.sup.2+]-regulated exocytosis, but not the [Ca.sup.2+] sensitivity. Moreover, under a condition of ATP depletion by dinitrophenol (DNP) or anoxia ([N.sub.2] bubbling), ACh evoked only a sustained phase in exocytotic events with no initial transient phase. However, ACh evoked an initial transient phase followed by a sustained phase with addition of cGMP before ATP depletion, whereas only a sustained phase was evoked in a case of cGMP addition after ATP depletion. Thus cGMP-induced enhancement in ACh-stimulated exocytotic events requires ATP, suggesting that cGMP modulates ATP-dependent priming of [Ca.sup.2+]-regulated exocytosis in antral mucous cells. In conclusion, cGMP increases the number of primed granules via acceleration of the ATP-dependent priming, which enhances the [Ca.sup.2+]-regulated exocytosis stimulated by ACh. gastric mucin secretion; guanosine 3'-cyclic monophosphate; exocytosis; acetylcholine; intracellular calcium concentration

Indomethacin (IDM, 10 μm), not aspirin (ASA; 10 μm), enhanced the Ca2+-regulated exocytosis stimulated by 1 μm acetylcholine (ACh) in guinea-pig antral mucous cells. Indomethacin inhibits prostaglandin G/H (PGG/H) and 15 R-hydroperoxy-eicosatetraenoic acid (15R-HPETE) production from arachidonic acid (AA), while ASA inhibits PGG/H production but accelerates 15R-HPETE production. This suggests that IDM accumulates AA. Arachidonic acid (2 μm) enhanced Ca2+-regulated exocytosis in antral mucous cells to a similar extent to IDM. Moreover, a stable analogue of AA, arachidonyltrifluoromethyl ketone (AACOCF3), also enhanced Ca2+-regulated exocytosis, indicating that AA, not products from AA, enhances Ca2+-regulated exocytosis. We hypothesized that AA activates peroxisome proliferation activation receptor α (PPARα), because AA is a natural ligand for PPARα. A PPARα agonist (WY14643; 1 μm) enhanced Ca2+-regulated exocytosis, and a PPARα blocker (MK886; 50 μm) abolished the enhancement of Ca2+-regulated exocytosis induced by AA, IDM, AACOCF3 and WY14643. Western blotting and immunohistochemical examinations demonstrated that PPARα exists in antral mucous cells. Moreover, MK886 decreased the frequency of Ca2+-regulated exocytosis activated by 1 μm ACh or 2 μm thapsigargin alone by 25–30%. Thus, ACh stimulates AA accumulation via an [Ca2+]i increase, which activates PPARα, leading to enhancement of Ca2+-regulated exocytosis in antral mucous cells. A novel autocrine mechanism mediated via PPARα enhances Ca2+-regulated exocytosis in guinea-pig antral mucous cells. [ABSTRACT FROM AUTHOR]

Indomethacin (IDM, 10 microm), not aspirin (ASA; 10 microm), enhanced the Ca(2+)-regulated exocytosis stimulated by 1 microm acetylcholine (ACh) in guinea-pig antral mucous cells. Indomethacin inhibits prostaglandin G/H (PGG/H) and 15R-hydroperoxy-eicosatetraenoic acid (15R-HPETE) production from arachidonic acid (AA), while ASA inhibits PGG/H production but accelerates 15R-HPETE production. This suggests that IDM accumulates AA. Arachidonic acid (2 microm) enhanced Ca(2+)-regulated exocytosis in antral mucous cells to a similar extent to IDM. Moreover, a stable analogue of AA, arachidonyltrifluoromethyl ketone (AACOCF(3)), also enhanced Ca(2+)-regulated exocytosis, indicating that AA, not products from AA, enhances Ca(2+)-regulated exocytosis. We hypothesized that AA activates peroxisome proliferation activation receptor alpha (PPARalpha), because AA is a natural ligand for PPARalpha. A PPARalpha agonist (WY14643; 1 microm) enhanced Ca(2+)-regulated exocytosis, and a PPARalpha blocker (MK886; 50 microm) abolished the enhancement of Ca(2+)-regulated exocytosis induced by AA, IDM, AACOCF(3) and WY14643. Western blotting and immunohistochemical examinations demonstrated that PPARalpha exists in antral mucous cells. Moreover, MK886 decreased the frequency of Ca(2+)-regulated exocytosis activated by 1 microm ACh or 2 microm thapsigargin alone by 25-30%. Thus, ACh stimulates AA accumulation via an [Ca(2+)](i) increase, which activates PPARalpha, leading to enhancement of Ca(2+)-regulated exocytosis in antral mucous cells. A novel autocrine mechanism mediated via PPARalpha enhances Ca(2+)-regulated exocytosis in guinea-pig antral mucous cells.

Background: Rosiglitazone, an insulin sensitizing agent, has been recently implicated in the control of inflammatory processes and modulation of expression of various cytokines such as tumor necrosis factor (TNF-α). However, its mechanistic effect of gastric mucosal integrity remains to be elucidated., Methods: The present study was designed to determine effect of rosiglitazone on gastric mucosal lesions induced by indomethacin (IND) in rats. Pyloric ligation was performed for the collection of gastric juice, and gastric ulceration was induced by a single intraperitoneal injection of IND (30 mg/kg)., Results: IND administration caused a significant decrease in the volume of gastric juice mucin and gastric mucosal nitrite and prostaglandin E 2 (PGE 2 ) levels. This was accompanied by a significant increase in gastric juice free and total acidity and pepsin activity. In addition, an elevation in the gastric mucosal lipid peroxide and serum TNF-α level was observed. Pretreatment with rosiglitazone (10 mg/kg, orally, for 1 weeks) resulted in a significant reduction in the elevated gastric mucosal lesions and lipid peroxides levels. This was associated with a marked increase in gastric juice mucin and a reduction in TNF-α level. Moreover, rosiglitazone significantly increased the gastric mucosal total nitrite and PGE 2 levels., Conclusions: Rosiglitazone exerts a gastroprotective effect against IND-induced gastric mucosal lesions and its anti-ulcer effect is mediated via scavenging free radicals, increasing NO, PGE 2 and mucus production in addition to its anti-inflammatory mechanisms. Thus, rosiglitazone could be a relevant drug for patients taking non-steroidal anti-inflammatory drugs (NSAIDs) and at high risk of developing gastric ulceration.