Diets Supplemented with Probiotics Improve the Performance of Broilers Exposed to Heat Stress from 15 Days of Age.

The poultry sector demands alternative additives to antibiotics that can be used as performance enhancers. Therefore, this experiment was conducted to evaluate the probiotics effects on performance, intestinal health, and redox status of 720 broilers exposed to heat stress from 15 days of age. Eight dietary treatments were evaluated: basal diet (BD) without antibiotic and probiotic (T1); BD supplemented with antibiotic zinc bacitracin (T2), BD supplemented with commercial probiotic of Bacillus subtilis DSM 17,299 (T3), BD supplemented with non-commercial probiotic of Lactococcus lactis NCDO 2118, Lactobacillus delbrueckii CNRZ 327, Escherichia coli CEC15, or Saccharomyces boulardii (T4 to T7), and BD simultaneously supplemented with the four non-commercial probiotics (T8). Feed intake, weight gain, and feed conversion were determined in the period from 1 to 42 days of age. Carcass and cuts yield, abdominal fat deposition, cloacal temperature, weight and length of intestine, activity of myeloperoxidase and eosinophilic peroxidase enzymes in the jejunum, jejunal histomorphometry, relative gene expression in the jejunum (occludin, zonulin, interleukin-8, cholecystokinin, ghrelin, and heat shock protein-70), and liver (heat shock protein-70), in addition to malondialdehyde level and superoxide dismutase activity in the intestine, liver, and blood, were measured in broilers at 42 days old. As main results, broilers fed T1 diet exhibited lower weight gain (3.222 kg) and worse feed conversion (1.70 kg/kg). However, diets containing non-commercial probiotics resulted in up to 3.584 kg of weight gain and improved feed conversion by up to 10%, similar to that observed for broilers of the T2 and T3 groups.

Protein-to-creatinine urinary in the early diagnosis of renal injury in canine pyometra / Relação proteína-creatinina-urinária no diagnóstico precoce de lesão renal em cadelas com piometra

Kidney disease that affects bitches with pyometra may lead patients to develop chronic renal failure even after pyometra treatment. Therefore, several studies have sought to clarify the gaps in the understanding of the pathogenesis of renal injury in pyometra. Identification of early detection markers for renal damage, which can predict and identify the prognosis of the disease, is very important. Proteinuria analysis can diagnose kidney damage, since proteins such as albumin are not filtered through the glomerulus and those that undergo glomerular filtration are almost completely reabsorbed by tubular cells. The objective of this study was to evaluate whether the urinary protein-to-creatinine ratio (UPC) can detect renal injury in bitches with pyometra before development of azotemia. For this, 44 bitches with pyometra were divided into two groups: bitches with azotemic piometra (A, n=15, creatinine >1.7) and bitches with non-azotemic pyometra (NA, n=29). The two groups were compared to the control group (CG, n=12), which had no signs of systemic disease. All animals underwent blood and urine tests. Leukocytosis was more evident in bitches in the A group than in the other groups. This shows that the inflammatory response may be associated with the pathogenesis of renal injury. The median UPC in bitches with pyometra was significantly higher than in the CG, with a median above the reference values. In conclusion, the UPC can be used in bitches with pyometra to detect renal damage before the development of azotemia. It has been suggested that the UPC of bitches with pyometra should be followed through during the postoperative period so that permanent renal lesions secondary to pyometra can be diagnosed and treated properly before the development of azotemia.(AU)

A doença renal que afeta cadelas com piometra pode levar a insuficiência renal crônica mesmo após o tratamento. Portanto, vários estudos procuraram esclarecer as lacunas na compreensão da patogênese da lesão renal na piometra. A identificação de marcadores de lesão renal precoce, que podem prever e identificar o prognóstico da doença é muito importante. A análise da proteinúria pode diagnosticar lesão renal, uma vez que proteínas como a albumina não são filtradas através do glomérulo e aquelas que sofrem filtração glomerular são quase completamente reabsorvidas pelas células tubulares. O objetivo deste estudo foi avaliar se a relação proteína-creatinina urinária (UPC) pode detectar lesão renal em cadelas com piometra antes do desenvolvimento de azotemia. Para isso, 44 cadelas com piometra foram divididas em dois grupos: cadelas com piometra azotêmica (A, n=15, creatinina >1,7) e cadelas com piometra não azotêmica (NA, n=29). Os dois grupos foram comparados ao grupo controle (CG, n=12), que não apresentaram sinais de doença sistêmica. Todos os animais foram submetidos a exames de sangue e urina. A leucocitose foi mais evidente nas cadelas do grupo A do que nos outros grupos. Isso mostra que a resposta inflamatória pode estar associada à patogênese da lesão renal. A mediana da UPC em cadelas com piometra foi significativamente maior que no CG, com uma mediana acima dos valores de referência. Em conclusão, a UPC pode ser usada em cadelas com piometra para detectar lesões renais antes do desenvolvimento de azotemia. Sugeriu-se que a UPC de cadelas com piometra deve ser acompanhada durante o pós-operatório, de modo que as lesões renais permanentes secundárias à piometra possam ser diagnosticadas e tratadas adequadamente antes do desenvolvimento de azotemia.(AU)

Moderate Treadmill Exercise Training Improves Cardiovascular and Nitrergic Response and Resistance to Trypanosoma cruzi Infection in Mice.

There is evidence suggesting that exercise training (ET) acts as a factor toward resistance to Trypanosoma cruzi infection. However, the effects of mean arterial pressure (MAP), heart rate (HR), and nitric oxide (NO) during the acute phase of infection has not been elucidated yet. Swiss mice were randomly assigned into four groups: sedentary control (SC, n = 30), trained control (TC, n = 30), sedentary infected (SI, n = 30), and trained infected (TI, n = 30). ET was performed on the treadmill for 9 weeks. After training, the mice were infected with 5 × 103 trypomastigotes of T. cruzi (Y strain) or PBS. We observed resting bradycardia and improved performance in trained animals compared with sedentary ones. On the 20th day post-infection (DPI), we found a decrease in HR in SI animals compared to TI animals (699.73 ± 42.37 vs. 742.11 ± 25.35 bpm, respectively, P < 0.05). We also observed increased production of NO in cardiac tissue on the 20th DPI in the SI group, normalized in TI group (20.73 ± 2.74 vs. 6.51 ± 1.19 µM, respectively). Plasma pro-inflammatory cytokines (IL-12, TNF-α, IFN-γ,) and MCP-1 were increased in SI animals, but decreased in TI animals. The increase in parasitemia on the 15th and 17th DPI in the SI group was attenuated in the TI group. Our results suggest that previous ET plays a preventive role in resistance to T. cruzi infection, modulating cardiovascular aspects, inflammatory reaction, and NO levels of infected mice.

Fish oil supplementation benefits the murine host during the acute phase of a parasitic infection from Trypanosoma cruzi.

Long-chain omega-3 polyunsaturated fatty acids (LC n-3 PUFA) are known to modulate a variety of immune cell functions. On occasion, this has led to diminished host resistance to certain viral and bacterial infections. Little is known about the impact of n-3 PUFA on host resistance to parasitic infection, however, based on results from a small study conducted more than two decades ago, we hypothesized that providing mice LC n-3 PUFA will diminish host resistance to Trypanosoma cruzi, the parasitic pathogen responsible for Chagas disease. To investigate this, C57BL/6 mice were supplemented by gavage (0.6% v/w) with phosphate-buffered saline, corn oil (CO), or menhaden fish oil (FO, a fat source rich in LC n-3 PUFA) for 15 days prior to T cruzi (Y strain) challenge and throughout the acute phase of infection. FO supplementation was associated with a transient 2-fold greater peak of blood parasitemia at 7 days postinfection (dpi), whereas subsequent cardiac parasitemia was ~60% lower at 12 dpi. FO treatment also ameliorated the leukopenia and thrombocytopenia observed in the early stages of a T cruzi infection. FO supplementation reduced circulating and cardiac nitric oxide at 7 and 12 dpi, respectively. FO supplementation altered ex vivo prostaglandin E2 and cytokine and chemokine production by splenocytes isolated from uninfected and infected mice. Overall, our results suggest that oral administration of LC n-3 PUFA from FO can have beneficial effects on the host in the early course of a T cruzi infection.

Inhibition of cyclooxygenase-1 and cyclooxygenase-2 impairs Trypanosoma cruzi entry into cardiac cells and promotes differential modulation of the inflammatory response.

The intracellular protozoan parasite Trypanosoma cruzi is the etiologic agent of Chagas disease, a serious disorder that affects millions of people in Latin America. Cell invasion by T. cruzi and its intracellular replication are essential to the parasite's life cycle and for the development of Chagas disease. Here, we present evidence suggesting the involvement of the host's cyclooxygenase (COX) enzymes during T. cruzi invasion. Pharmacological antagonists for COX-1 (aspirin) and COX-2 (celecoxib) caused marked inhibition of T. cruzi infection when rat cardiac cells were pretreated with these nonsteroidal anti-inflammatory drugs (NSAIDs) for 60 min at 37°C before inoculation. This inhibition was associated with an increase in the production of NO and interleukin-1ß and decreased production of transforming growth factor ß (TGF-ß) by cells. Taken together, these results indicate that COX-1 more than COX-2 is involved in the regulation of anti-T. cruzi activity in cardiac cells, and they provide a better understanding of the influence of TGF-ß-interfering therapies on the innate inflammatory response to T. cruzi infection and may represent a very pertinent target for new therapeutic treatments of Chagas disease.

Antioxidant effect of N-acetylcysteine on prehepatic portal hypertensive gastropathy in rats.

BACKGROUND: Portal hypertension is a clinical syndrome associated with the development of a hyperdynamic circulation and gastroesophageal varices. Aim. To evaluate the antioxidant effect of N-acetylcysteine on portal hypertensive rats. MATERIAL AND METHODS: Portal hypertension was induced by partial portal vein ligation (PPVL). Oxidative damage in the stomach was measured by lipoperoxidation trough thiobarbituric acid reactive substances (TBARS) and antioxidant enzyme activity; we also evaluated nitrates and nitrites level and histology stained by hematoxylin-eosin. We performed evaluation of portal pressure and measurement of vessels diameter. Liver damage was evaluated by measuring hepatic enzymes. The animals were divided in four experimental groups (n = 6): Sham-operated (SO), SO + NAC, Partial portal vein ligation (PPVL) and PPVL + NAC. N-acetylcysteine (10 mg/kg ip) was administered daily for 7 days and started 8 days after surgery. RESULTS: The portal hypertensive group showed an increase in portal pressure, vessels diameter, levels of TBARS and nitrates and nitrites when compared to SO group. These values were accompanied by a decrease in superoxide dismutase (SOD) and glutathione peroxidase (GPx) antioxidant enzyme activity. Histology showed dilated vessels in the gastric mucosa in the PPVL group. NAC was able to decrease portal pressure values, vessels diameter, TBARS and also nitrates and nitrites levels when compared to PPVL group. Furthermore, PPVL+NAC group presented an increase in SOD and GPx activity. N-acetylcysteine attenuated damage in gastric mucosa. CONCLUSION: Oxidative stress is associated with portal hypertension and that antioxidant NAC is able to minimize damages of PPVL in rats.

Supplementation of coenzyme Q10 and alpha-tocopherol lowers glycated hemoglobin level and lipid peroxidation in pancreas of diabetic rats.

The importance of nutritional supplementation in diabetes remains an unresolved issue. The present study was undertaken to examine the effects of alpha-tocopherol and CoQ(10), powerful antioxidants, on metabolic control and on the pancreatic mitochondria of GK rats, a model of type 2 diabetes. We also evaluated the efficacy of these nutrients in preventing the diabetic pancreatic lesions observed in GK rats. Rats were divided into 4 groups, a control group of diabetic GK rats and 3 groups of GK rats administered with alpha-tocopherol and CoQ(10) alone or both in association, during 8 weeks. Fasting blood glucose levels were not significantly different between the groups, nor were blood glucose levels at 2 hours after a glucose load. HbA1c level was significantly reduced in the group supplemented with both antioxidants. Diabetes induced a decrease in coenzyme Q plasma levels that prevailed after treatment with antioxidants. In addition, the plasma alpha-tocopherol levels were higher after treatment with the antioxidants. An increment in some components of the antioxidant defense system was observed in pancreatic mitochondria of treated GK rats. Moreover, the antioxidants tested either alone or in association failed to prevent the pancreatic lesions in this animal model of type 2 diabetes. In conclusion, our results indicate that CoQ(10) and alpha-tocopherol decrease glycated HbA1c and pancreatic lipid peroxidation. These antioxidants increase some components of the antioxidant defense system but do not prevent pancreatic lesions. Thus, we cannot rule out the potential benefit of antioxidant treatments in type 2 diabetes in the prevention of their complications.

Histological changes and impairment of liver mitochondrial bioenergetics after long-term treatment with alpha-naphthyl-isothiocyanate (ANIT).

This study was designed to evaluate the effects of long-term treatment with alpha-naphthyl-isothiocyanate (ANIT) on liver histology and at the mitochondrial bioenergetic level. Since, ANIT has been used as a cholestatic agent and it has been pointed out that an impairment of mitochondrial function is a cause of hepatocyte dysfunction leading to cholestatic liver injury, serum markers of liver injury were measured and liver sections were analyzed in ANIT-treated rats (i.p. 80 mg/kg/week x 16 weeks). Mitochondrial parameters such as transmembrane potential, respiration, calcium capacity, alterations in permeability transition susceptibility and ATPase activity were monitored. Histologically, the most important features were the marked ductular proliferation, proliferation of mast cells and the presence of iron deposits in ANIT-treated liver. Mitochondria isolated from ANIT-treated rats showed no alterations in state 4 respiration, respiratory control ratio and ADP/O ratio, while state 3 respiration was significantly decreased. No changes were observed on transmembrane potential, but the repolarization rate was decreased in treated rats. Consistently with these data, there was a significant decrease in the ATPase activity of treated mitochondria. Associated with these parameters, mitochondria from treated animals exhibited increased susceptibility to mitochondrial permeability transition pore opening (lower calcium capacity). Since, human cholestatic liver disease progress slowly overtime, these data provide further insight into the role of mitochondrial dysfunction in the process.

[Morphological changes of islet of Langerhans in an animal model of type 2 diabetes]. / Alterações da morfologia do ilhéu de Langerhans na evolução da síndrome diabética num modelo animal de diabetes tipo 2.

The impairment of insulin secretion, a major feature of type 2 diabetes, is caused by beta-cell mass reduction and functional failure. Pancreatic beta-cell mass reduction is variable in humans, not exceeding 50%, and has been associated with amyloid deposits. In the present study, we have chronologically compared the endocrine pancreas morphology of Wistar control rats (W) and Goto-Kakizaki (GK) rats, an animal model of non obese type 2 diabetes. We have also characterised and compared their body weight, glycaemia (fasting and after oral glucose load) as well as other biochemical parameters. GK rats were always glucose intolerant and fasting hyperglycaemia arised at four week of age. Wistar rats had mild glucose intolerance in their first two weeks of life. GK rats had a total beta-cell mass always decreased when compared to controls, but above 40%. In adult GK rats (12 weeks old) alterations in the architecture of a sub-population of islets occurred which displayed signs of prominent fibrosis, with cluster of beta-cells widely separated by strands of connective tissue and deposits of PAS positive material. Our findings demonstrate that, using GK rats from the Coimbra colony, beta-cell mass reduction is one of the primary features in the pathological sequence leading to diabetes. Structural lesions of the islets, that will further increase beta-cell mass reduction and compromise beta-cell function, will appear latter mainly due to hyperglycaemia.