Developmental changes in frontocortical morphology and neurochemistry of neonatal rats following gestational nicotine exposure

Exposure of the embryo or foetus to nicotine during development results in some forms of neurological deficits later in life. The current study aimed at determining the effects of prenatal nicotine administration during the 1st and 2nd gestational weeks on the frontal cortex of neonatal Wistar rats. For each week of gestation, pregnant Wistar rats were assigned to 3 groups: a control group (1), and two treated groups (2 and 3), and were given intra-peritoneal nicotine at 6.88 mg/ kg and 13.76 mg/kg doses respectively. The weights of the litters were taken at birth and at postnatal day 4; the whole brain and frontal cortical weights were also assessed. Tissues for histological demonstration were fixed in freshly prepared formol calcium, while specimen for biochemical studies were homogenised and processed for the determination of alkaline phosphatase (ALP) and malondialdehyde (MDA) activities. Findings in the treated animals showed low birth weights, raised ALP but reduced MDA, with corresponding alterations in the cortical cytoarchitecture, which could explain some of the pathological basis for the neurobehavioural problems associated with offspring of women smokers.Keywords: Prenatal nicotine, Frontal cortex, Morphology, Histology, ALP, MD

Moringa Regimen Corrects Nicotine-induced Deficits in Behaviour, Altered Energy Metabolism and Neurotransmitter Processing in Rat Brain

Background: Nicotine is the addictive component of tobacco smoking. It has been reported to have a negative neuromodulatory role in the CNS. Moringa oleifera is a medicinal plant with reported antioxidant, anticonvulsant, anti-inflammatory and neuroprotective properties. Aim and Objectives: This study was purposed to investigate the neuronal adaptation potentials of Moringa Oleifera (MO) on nicotine induced behavioural decline and perturbed bioenergetics. Material and Methods: Twenty-four adult male Wistar rats were used. The treatment regimen was as follows; control group received distilled water, MO group received 200 mg/kg of MO, Nicotine Group received 1.38 mg/kg body weight of nicotine, and Nicotine + MO group received combined treatment of 200 mg/kg body weight of MO after 1.38 mg/kg body weight of nicotine for 28 days. The animals were subjected to Morris water maze for spatial memory, Y maze for working memory and elevated-plus maze tests for anxiety levels after which they were sacrificed for spectrophotometric analysis of global protein expression, neural bioenergetics (lactate dehydrogenase and glucose-6-phosphate dehydrogenase), and Acetylcholinesterase (AChE) levels. Results: Nicotine infusion caused a reduction in the escape latency period, increased the percentage incorrect alternation, and elevated the anxiety levels of rats. These observations were indicative of decreased synaptic activity in the brain. Together with, nicotine induced chromatolytic changes in cells of the frontal cortex and hippocampus. Co-administration with MO prevented nicotine-associated memory decline, perturbed glucose bioenergetics, induced chromatolysis and histomorphological distortion in the frontal cortex and hippocampus. Conclusion: Our data demonstrate that MO administration enhances experience-dependent neuroplasticity and cognitive behaviour function in laboratory animals, modulates energy metabolism and reduced oxidant stress possibly through enhanced production of key antioxidant enzymes against the damaging effects of nicotine. It provided evidence that MO can be further developed as a means to protect the brain from oxidative stress-induced injury

Evaluation of the effects of ascorbic acid on azathioprine-induced alteration in the testes of adult Wistar rats

The use of azathioprine (AZA) in the prevention of organ rejection during transplantation has been noted in different organs of the body. This study investigates the effect of ascorbic acid on azathioprineinduced alteration in the testes of adult Wistar rats. Thirty male adult Wistar rats were randomly assigned into 5 groups comprising a Control group A and four Treatment groups B to E. Animals in treatment groups B and D received 10 and 20 mg/kg of AZA respectively; whilerats in treatment groups C received 10 mg/kg AZA +25 mg/kg ascorbic acid, and group E received 20 mg/kg of AZA + 50 mg/kg of ascorbic acid. The control group animals received equal volume of normal saline via orogastric tube, and treatment lasted for 21 days. The testes were excised, weighed and fixed in Bouins’ fluid fortissue histology. Tissue homogenate was used to assay testosterone level, while blood was also obtained intracardially for glutathione peroxidase studies. Findings revealed significant histological changes in the treatment groups, decreased testosterone levels, and elevated glutathione peroxidase activity in all the treatment groups, compared with control. However, the treatment groups that received ascorbic acid had minimal, butsignificant reduction in the glutathione peroxidase activity compared to treatment groups without ascorbic acid intervention. Use of azathioprine induces significant damage to testicular structure, and this cannot be ameliorated by the use of ascorbic acid

Liver enzymes derangement and the influence of diet in animals given oral albendazole

Background: Albendazole is used as an anthelmintic in the treatment of some parasitic infections. This study determined how the effects of albendazole on liver enzymes are influenced by diet. Materials and Method: Thirty adult male Wistar rats of mean weight 304.12 ± 11.34 g were randomly grouped into five: Group A: Control, was given rat pellets and water only; Group B received 15 mg/kg/d of albendazole while fasting; Group C received 15 mg/kg/d of albendazole with fatty meal; Group D received 15 mg/kg/d of albendazole with normal diet (rat pellets); and, Group E received 30 mg/kg/d of albendazole with normal diet (rat pellets); they were given orally for 3 consecutive days. The animals were sacrificed thereafter and blood samples obtained for quantitative study of the serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). Results: Significant elevation in the serum levels of the transaminases especially in animals which were on their normal diet (rat pellets), while ALP was either reduced or increased based on dietary factors. Conclusions: Oral administration of albendazole before meal or with a fatty diet could help limit severe elevation of liver enzymes associated with its use, while still ensuring optimal efficacy

Lipid Profile and Liver Histochemistry in Animal Models Exposed to Cigarette Smoke

Cigarette smoke is known to be an important predisposing factor to many diseased conditions, such as cardiovascular diseases, liver disease, atherosclerosis and other metabolic disorders. The aim of this study was to examine the effects of exposure to smoke from burnt cotton wool and cigarette on plasma lipids, liver biochemistry and histology, in adult Wistar rats. The animals were divided into three groups of Control A: exposed to fresh atmospheric air; Group B: exposed to cotton wool smoke; and, Group C, exposed to cigarette smoke; and the experiment lasted for 35 days. The animals exposed to cigarette smoke and cotton wool smoke showed higher values of low density lipoprotein (LDL), and lower values of high density lipoprotein (HDL) compared to the control. The observation of the micro architecture and enzymes of the liver tissue revealed reduction in the number and size of liver cells, numerous fibrous tissues, elevated liver transaminases and reduction in endogenous anti-oxidants, with evidence of fatty degeneration, in animals exposed to cigarette smoke compared to those exposed to cotton wool smoke and fresh atmospheric air. Cigarette smoke caused accumulation of lipids in the liver cells, with evidence of on-going necrosis and fibrosis, which indicated the presence of non-alcoholic fatty liver disease

Lipid Profile and Liver Histochemistry in Animal Models Exposed to Cigarette Smoke

Cigarette smoke is known to be an important predisposing factor to many diseased conditions, such as cardiovascular diseases, liver disease, atherosclerosis and other metabolic disorders. The aim of this study was to examine the effects of exposure to smoke from burnt cotton wool and cigarette on plasma lipids, liver biochemistry and histology, in adult Wistar rats. The animals were divided into three groups of Control A: exposed to fresh atmospheric air; Group B: exposed to cotton wool smoke; and, Group C, exposed to cigarette smoke; and the experiment lasted for 35 days. The animals exposed to cigarette smoke and cotton wool smoke showed higher values of low density lipoprotein (LDL), and lower values of high density lipoprotein (HDL) compared to the control. The observation of the micro architecture and enzymes of the liver tissue revealed reduction in the number and size of liver cells, numerous fibrous tissues, elevated liver transaminases and reduction in endogenous anti-oxidants, with evidence of fatty degeneration, in animals exposed to cigarette smoke compared to those exposed to cotton wool smoke and fresh atmospheric air. Cigarette smoke caused accumulation of lipids in the liver cells, with evidence of on-going necrosis and fibrosis, which indicated the presence of non-alcoholic fatty liver disease