Fibre Characterization of Cassava Peel Leaf Meal and Its Utilization by Broilers

One hundred and twenty ( n = 120) day old broiler chicks with an average weight (100.00±7.00g) were randomly allotted to four dietary treatments, with cassava peel leaf meal (CPLM) as replacement for maize at (starter and finisher phases).The trial was in three phases of adaptation  (1-2week),starter (3-5week) and finisher (6-9week).Thirty broilers chicks were assigned to each of the four treatments, while was replicated three times at 10 chicks each. Performance of the chicks such weight gain, feed intake and carcass yield was evaluated and the proximate and fiber quality of the diets and CPLM were also determined. Data obtained for performance evaluated was analyzed using ANOVA, while significant means were separated by SAS of the same package. The outcome revealed that CPLM had (89.93%) dry matter, (18.93%) crude protein and (43.28%) NDF, with anon-significant (p< 0.05) variation in weight gain, enhanced (p< 0.05) feed intake and depressed (p< 0.05) feed to gain ratio as CPLM inclusion increased. Dressing percentage values (69.00-73.00%) were obtained on the treatments. CPLM inclusion (0, 15, 30 and 45%) as replacement for maize in the diets of broilers produced a favourable performance. Keywords: Cassava peel, cassava leaf, fiber, broiler chick

Nigella sativa oil attenuates aluminum-induced behavioral changes, oxidative stress and cortico-hippocampal neuronal degeneration in rats

Background: Aluminum (AlCl3) usage in both the industrial and domestic arena has dramatically risen over time owing to its ubiquity and utility for many activities despite frequent reporting of its neurotoxic effects over wide range of concentrations. The neuro-protective effects of Nigella sativa Oil (NSO) following intermediate exposure to aluminum salts has largely been unexplored. The present study explores the ameliorative and neuro-protective functions of NSO on aluminum chloride (AlCl3)-induced damages in the frontal cortices and hippocampus of exposed rats. Methods: The study involved the use of thirty two adult male Wistar rats weighing 180 ± 20 g, randomly divided into four groups, in which group 1 received saline, group 2 received AlCl3 (100 mg/kg), group 3 received AlCl3 (100 mg/kg) followed by NSO (1 ml/kg) 30 min later, while group 4 received NSO (1 ml/kg) only. All administrations were done orally for 14 days. Standardized behavioural tests for anxiety and cognitive performance were carried on after the treatments prior to euthanizing (Ketamine 10 mg/kg, ip). On day 15, the rats were euthanized, and their brains excised, with the frontal cortex and hippocampus removed. Five of these samples were homogenized and centrifuged to analyze nitric oxide (NO) metabolites and total reactive oxygen species (ROS), and the other three were processed for histology (cresyl violet stain) and proliferative markers (Ki-67 immunohistochemistry). Results: Increased Transfer latency, time in dark box, escape latency and reduced rearing frequency, percentage alternation and time in platform quadrant were observed in the AlCl3 exposed rats. There was also an increased level of ROS and NO in the brain regions with marked inhibition of neuronal cell proliferation as evidenced by reduced Ki-67 protein expression in the brain of AlCl3 only rats. However, rats co-administered AlCl3 and NSO showed significantly reduced ROS and NO levels, improved anxiety-like and cognitive behaviors and increased Ki-67 expression when compared with AlCl3 only treated rats. Conclusion: AlCl3 exposure causes neuronal damage and impaired anxiety-like and memory indices which are associated with increased free radical generation and inhibited neuronal proliferation, whereas the antioxidant and neuro-protective properties of NSO were efficacious against the observed effects. Keywords: Aluminum chloride, memory impairment, neuronal damage, Ki-67, nigella sativa oi