Effects of dietary supplementation of synbiotics and phytobiotics on performance, caecal coliform population and some oxidant/antioxidant parameters of broilers.

The current study was conducted to evaluate the effects of dietary supplementation of synbiotics and phytobiotics on performance, small intestine weight, pH and caecal coliform counts of broilers. The influences of synbiotics and phytobiotics on oxidant/antioxidant status in the blood of broilers were also assessed. A total of 200 broiler chicks were randomly allotted to four dietary treatments, either fed a basal diet or the same diet supplemented with 1 g/kg synbiotic, 1 g/kg phytobiotic or 1 g/kg synbiotic plus 1 g/kg phytobiotic. The diet supplemented with both synbiotic and phytobiotic had no effect on body weight, body weight gain, feed intake and feed efficiency of broilers at the end of the study (p > 0.05). Neither small intestine weight nor pH was affected by any of the treatments. Supplementation of both synbiotic and phytobiotic to diet decreased the caecal coliform count (p < 0.01). Addition of synbiotics and phytobiotics in combination significantly increased plasma malondialdehyde (MDA) levels (p ≤ 0.05), whereasphytobiotic addition alone showed only a slight increase. Similarly, elevated nitric oxide (NO) level was recorded in the synbiotic- and phytobiotic-fed group and in the phytobiotic-fed group (p ≤ 0.001). Superoxide dismutase (SOD) activities did not differ between the groups. In conclusion, dietary supplementation of synbiotic and phytobiotic improved the gut health by decreasing the caecal total coliform count, but growth performance was not affected by the supplementations. Further investigations are needed to determine the effects of phytobiotics on oxidative/antioxidative metabolism as regards their compositional analysis.

Elevated cAMP levels reverse Brucella melitensis-induced lipid peroxidation and stimulate IL-10 transcription in rats.

Brucella species are able to survive and replicate within the phagocytic vacuole of macrophages that induce chronic infection in humans and domestic animals. The activation of oxidative bactericidal activity is one of the defense systems which protect the host from the toxic effects of pathogens. The aim of this study was to evaluate lipid peroxidation, NO production, antioxidative system and inflammation during a period of brucella infection in a rat model; in addition to investigate the role of elevated intracellular cyclic AMP on Brucella-induced events. Brucella significantly induced lipid peroxidation in plasma, liver and spleen by 3-5-fold at 7 days postinfection. NO concentration was significantly elevated in the liver and spleen while unchanged in plasma. Cyclic AMP elevating agent, rolipram, administration (1mg/kg/day i.p., 3 days) gradually suppressed lipid peroxidation and NO formation to the basal level in plasma and spleen whilst only a slight decrease was observed in liver. Brucella considerably decreased SOD activity in the liver and spleen, with rolipram restoring the enzyme activity in liver and activity in spleen being unchanged. Reverse transcriptase PCR analyses showed that Brucella melitensis does not alter TNF-alpha and IFN-gamma transcriptions in liver and spleen. The pathogen did not consistently induce nitric oxide synthase mRNA transcriptions in animals; even in those housed in the same group. IL-10 transcription was induced by rolipram in spleen but not in liver. Our results suggest that activation of the cAMP/PKA pathway suppressed lipid peroxidation and the elevated NO concentrations caused by B. melitensis. Moreover, rolipram induced anti-inflammatory cytokine IL-10 transcription and SOD activity, albeit in a tissue dependent manner.