Thioacetamide (TAA) is a potent hepatotoxicant in acute and chronic hepatic injury. The study examined the protective effect of sesame oil against TAA-induced hepatic injury in rats. Hepatic injury was induced by intraperitoneal injection of 100 mg/kg of TAA for 24 h. Triple doses of sesame oil (1, 2, or 4 mL/kg) was given orally 0, 6, and 12 h after TAA treatment. TAA significantly increased serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Sesame oil decreased serum AST and ALT levels and significantly inhibited hepatic lipid peroxidation and nitric oxide levels compared with TAA-alone group. Further, sesame oil significantly inhibited TAA-induced hepatic neutrophil activation marker myeloperoxidase activity. However, sesame oil did not affect hepatic tumor necrosis factor, IL-1β and IL-10 generation in TAA-treated group. In conclusion, sesame oil protects against TAA-induced hepatic injury and oxidative stress via the inhibition of neutrophil activation. However, inflammatory cytokines may not be involved in sesame-oil-associated hepatic protection against TAA in rats.
Authors:Cezary Skobowiat, Jarosław Calka, Krzysztof Wasowicz, and Mariusz Majewski
Sympathetic chain ganglia (SChG) neurons projecting to the descending colon of the pig were studied by means of retrograde tracing (Fast Blue, FB) and double-labelling immunofluorescence methods. FB was injected into the gut wall and after three weeks survival time the animals were transcardially perfused with paraformaldehyde and the bilateral sympathetic trunks were collected. The FBpositive neurons were localised only in the lumbar (L
) ganglia of the sympathetic trunk and appeared either as small (30–50 μm in diameter) round-shaped perikarya forming clusters localised in caudal-ventral area or, rarely, as bigger (50–80 μm) and dispersed solitary irregular perikarya. Immunohistochemical staining revealed the catecholaminergic (tyrosine hydroxylase-/dopamine β-hydroxylase-immunoreactive) character of the great majority of FB-positive neurons which preferentially co-expressed neuropeptide Y. In addition, none of the FB-positive perikarya was immunopositive to galanin, somatostatin, choline acetyltransferase, vasoactive intestinal peptide, pituitary adenylate cyclase-activating peptide, leu
-enkephalin, nitric oxide synthase, substance P and calcitonin-generelated peptide.
Authors:Behnam Ahmadipour, Mohammadreza Sharifi, and Fariborz Khajali
This study assessed the preventive effects of arginine (ARG) and guanidinoacetic acid (GAA) on the incidence of pulmonary hypertension syndrome (PHS) in broiler chickens. Four isoenergetic and isonitrogenous diets were prepared, including: (i) the control, (ii) the control supplemented with 1 g/kg ARG, (iii) the control supplemented with 1 g/kg GAA, and (iv) the control supplemented with 1.5 g/kg GAA. These diets were fed to broilers (Ross 308) from day 1 to 42 post-hatch. Criteria evaluated in the experiment were growth performance, carcass characteristics, serum and blood variables, lead-II electrocardiogram, and ET-1 and iNOS gene expression in heart and lungs. Mortality from PHS was recorded daily. The results showed that ARG and GAA supplements improved the feed conversion ratio (FCR) compared to the control (P < 0.05). Supplementation of ARG and GAA significantly (P < 0.05) increased serum nitric oxide (NO) concentration. ARG and GAA supplementation significantly reduced the haematocrit value and the heterophil to lymphocyte ratio in the blood. A significant (P < 0.05) decline in S-wave amplitude of the lead-II electrocardiogram, right to total ventricular weight ratio (RV:TV) and ascites mortality was observed by supplementing ARG or 1.5 g/kg GAA. Addition of ARG and GAA supplements did not significantly change ET-1 and iNOS gene expression in the heart and lung relative to the control. In conclusion, GAA supplementation at 1.5 g/kg had a potential to improve growth performance and could prevent PHS.
Authors:SO Bashir, H Suekit, AO Elkarib, MA Dafaalla, MB Abd Elrouf, MD Morsy, and M Eskandar
KA , Taudorf S , James PE , McEneny J , Young IS , Swenson ER , Mairbäurl H , Bärtsch P , Berger MM : High-altitude pulmonary hypertension is associated with a free radical-mediated reduction in pulmonary nitricoxide