14 research outputs found
Effect of Essential Oils from Ginger (Zingiber officinale) and Turmeric (Curcuma longa) Rhizomes on Some Inflammatory Biomarkers in Cadmium Induced Neurotoxicity in Rats
Studies have revealed that anti-inflammatory agents could provide beneficial effect in lowering the incidence/progression of neurological diseases. Hence, this study sought to investigate the effect of essential oils from Nigeria ginger and turmeric rhizomes on some cytokines in cadmium induced neurotoxicity. The result revealed that essential oil from ginger and turmeric rhizomes exerts anti-inflammatory effect by preventing alterations of some cytokines/inflammatory biomarkers (IL-6, IL-10 and TNF-Alpha) levels and inhibits both hippocampus and prefrontal cortex acetylcholinesterase (AChE) and adenosine deaminase (ADA) activities (important enzymes relevant in the management/prevention of neurodegenerative diseases) in Cd treated rats. In conclusion, essential oil from ginger and turmeric rhizomes exerts anti-inflammatory properties in Cd induced neurotoxicity. The observed effect could be due to the volatile compounds as revealed by GC-MS analysis
The Cytoarchitectural alterations in the neocortex of Wistar rats: Effects of aqueous tobacco (Nicotiana tabacum) leaves extract exposure Adeniyi
This study investigated the effects of corresponding 11.7 mg/kg body weight and 5.8 mg/kg body weight/day of the tobacco leaves aqueous extract for a period of 20 days on the functions of rats’ brain after extract administration. Nicotiana tabacum is the scientific name of the tobacco plant grown in several countries of the world. It has been used in variables ways such as smoking, snuffing, even chewing, etc. 24 young rats of both sexes were used. They were divided into 3 groups, A, B, C of 8 rats each (Female (n = 4) and male (n = 4)). Group A were given 11.7 mg of the extract per kg body weight, group B 5.8 mg of the extract per kg body weight in 0.5 ml of distilled water per day throughout the 20 experimental days while group C were given equal volume (0.5 ml) of distilled water as well. The rats were sacrificed at day 21 by cervical dislocation and the brains were excised and fixed in formol calcium for 4 days and processed using Haematoxylin and Eosin staining method and Cresyl Fast Violet (CFV) staining technique. There was a statistical significant decrease in the body weight, brain weight and relative brain weight between groups A and B compared to the control group (p < 0.05). There was enlargement of the somata in the group A administered with 11.7 mg/kg B.Wt per day of the extract while those in group B appeared more spindle compared to those cells in group C. Also, the non – homogenous appearance of myelinated neocortex of the neuropil appear clearly in the treated groups compared to control (Figure 3). Therefore, the results suggested that the consumption of the aqueous extract of N. tabacum leaves may alter the normal functions of the brain which may lead to brain dysfunction, despite its “pleasant” effects and also help in reduction in weight gain.Key words: Nicotiana tabacum, cerebrum, frontal lobe, cytoarchitecture, neocortex
Cadmium Increases the Sensitivity of Adolescent Female Mice to Nicotine-Related Behavioral Deficits
This study investigates spatial and nonspatial working memory, anxiety related behavior, and motor activities in cadmium and/or nicotine exposed female adolescent mice. P28 female adolescent mice (albino strain) were divided into four groups of five (n=5) mice each. A set of mice (Nic) received subcutaneous nicotine (2.0 mg/kg) while a separate set (Cd) was treated with 2.0 mg/kg cadmium (subcutaneous). For the combined treatments of cadmium and nicotine, we administered 2.0 mg/kg Nicotine and 2.0 mg/kg of Cd. Subsequently, a separate group of animals (n=5; control) received normal saline. The total duration of treatment for all groups was 28 days (P28–P56). At P56, the treatment was discontinued, after which the animals were examined in behavioural tests. Nicotine and cadmium increased the metabolism and food intake in the female adolescent mice. This also corresponded to an increase in weight when compared with the control. However, a combined nicotine-cadmium treatment induced a decline in weight of the animals versus the control. Also, nicotine administration increased the motor function, while cadmium and nicotine-cadmium treatment caused a decline in motor activity. Both nicotine and cadmium induced a reduction in memory index; however, nicotine-cadmium treatment induced the most significant decrease in nonspatial working memory
P53, Bax and Cathepsin D Dysregulation in Neurons Subjected to Cyanide Toxicity and Oxygen Deprivation
Cyanide is a potent neurotoxin capable of potentiation NMDA R1 (N-methyl-D-aspartate receptor 1) a form of
glutamate receptor that is calcium gated, thus causing excitotoxicity. It is also well established that the
glutamate-glucose exchange is dependent on the activity of the Na
+
/K
+
ATPase pump, thus we examine the role
of the Na
+
/K
+
pump in the metabolism of the neuron during cyanide toxicity. Six separate perfusion set up of the
rat brain cortical tissues were made with ACSF (ACSF, ACSF+KCN, ACSF+KCN + pump blocker, ACSF + pump
blocker). The tissues were perfused for duration of 180 minutes. The tissues were processed
immunohistochemically using antibodies against p53,Bax and Cathepsin D (CD) to demonstrate disregulation of
cell cycle proteins associated with the induced DNAbreakage as a result of cyanide toxicity. The pumpblockers
(methyldigoxin and promethazine) induced excitotoxicity when used in culture, and amplified cyanide toxicity
when combined with KCN. Cell death induced by toxicity of cyanide and the blockade of the Na/K ATPasepump
has been seen to be complimentary in driving the toxicity effects that drives the cell into apoptosis.The tumor
suppressor/apoptosis inducing factors p53 and Bax were over expressed while cathepsin was suppressed to
show that the cells are apoptotic as against an increased cathepsin D level that would have implied senescence
Basic Principles of Fluorescence Microscopy
Fluorescence
microscopy is a basic requirement in cell biology
, molecular
biology
and
biotechnology
.
Advancements over the years has helped scientist to
trace molecules in live cells and understand the
basis of cell metabolism, exchange, mutation and to
xicity. In this short communication we seek to
explain in simple terms the basic principles of how
a fluorescence microscope works. The principles o
f
excitation and emission focuses on the ability of f
luorophores to absorb energy from photons and to
emit such absorbed energy. The difference between t
he chemical structures of these fluorephores
determines how much energy that is required to exci
te them and how long a fluorescence signal from a
fluorophore will last. The principles of epi-illumi
nation on the other hand describe the arrangement a
nd
function of the various components of a fluorescenc
e microscope
Motor and memory function in rat models of cyanide toxicity and vascular occlusion induced ischemic injury
Although oxidative stress is characteristic of global vascular occlusion and cyanide toxicity, the pattern of cerebral metabolism reconditioning
and rate of progression or reversal of neural tissue damage differ for both forms of ischemia. Thus, it is important to compare cognitive and
motor functions in both models of ischemia involving cyanide treatment (CN) and vascular occlusion (VO).
Adult Wistar rats (N = 30) were divided into three groups; VO (n = 12), CN (n = 12) and Control-CO (n = 6). The CN was treated with
30 mg/Kg of potassium cyanide (KCN); VO was subjected to global vascular occlusion-both for duration of 10 days. The control (CO) was
fed on normal rat chow and water for the same duration. At day 10, the test and control groups (CN, VO and CO) were subjected to motor
function tests (Table edge tests and Open Field Test) and memory function tests (Y-Maze and Novel object recognition) while the withdrawal
groups CN-I and VO-I were subjected to the same set of tests at day 20 (the withdrawal phase).
The results show that both cyanide toxicity and vascular occlusion caused a decline in motor and memory function when compared with
the control. Also, the cyanide treatment produced a more rapid decline in these behavioral parameters when compared with the vascular
occlusion during the treatment phase. After the withdrawal phase, cyanide treatment (CN-I) showed either an improvement or restoration of
motor and memory function when compared to the CN and control. Withdrawal of vascular occlusion caused no improvement, and in some
cases a decline in motor and memory function.
In conclusion, cyanide toxicity caused a decline in motor and memory function after the treatment while vascular occlusion caused no
significant decline in cognition and motor function at this time. After the withdrawal phase, the effect of cyanide toxicity was reduced and
significant improvements were observed in the behavioral tests (motor and cognitive), while a decline in these functions were seen in the
vascular occlusion group after this phase.
© 2014 Elsevier Ireland Ltd. All rights reserved
Nicotine-Cadmium Interaction Alters Exploratory Motor Function and Increased Anxiety in Adult Male Mice
In this study we evaluated the time dependence in cadmium-nicotine interaction and its effect on motor function, anxiety linked
behavioural changes, serum electrolytes, and weight after acute and chronic treatment in adult male mice. Animals were separated
randomly into four groups ofn= 6 animals each. Treatment was done with nicotine, cadmium, or nicotine-cadmium for 21 days.
A fourth group received normal saline for the same duration (control). Average weight was determined at 7-day interval for the
acute (D1-D7) and chronic (D7-D21) treatment phases. Similarly, the behavioural tests for exploratory motor function (open field
test) and anxiety were evaluated. Serum electrolytes were measured after the chronic phase. Nicotine, cadmium, and nicotinecadmium treatments caused no significant change in body weight after the acute phase while cadmium-nicotine and cadmium
caused a decline in weight after the chronic phase. This suggests the role of cadmium in the weight loss observed in tobacco smoke
users. Both nicotine and cadmium raised serum Ca
2+
concentration and had no significant effect on K
+
ionwhencomparedwith
the control. In addition, nicotine-cadmium treatment increased bioaccumulation of Cd
2+
in the serum which corresponded to a
decrease in body weight, motor function, and an increase in anxiety
Light microscopic detection of Plasmodium falciparum in vitro through Pf histidine rich protein 2 (HRP 2) gold conjugate labeling: Rapid diagnosis of cerebral malaria in humans
Plasmodium falciparum (Pf) has been found to be the deadliest of all the known species of the parasite
capable of infecting humans; this is because it is capable of causing severe cerebral tissue damage.
This study was carried out to demonstrate the parasite in the host blood in vitro through immunogold
labeling using antibodies against Plasmodium falciparum histidine rich protein 2 (HRP 2); a major metabolite released during the cause of the parasite infection and feeding in the erythrocyte. 12 known Pf positive samples were obtained from across the six geopolitical zones of Nigeria and were further
characterized by Geimsa thick and thin film for parasite identification parasite count expressed as
parasites/l of blood. An average of 400 parasites/l of blood was obtained in each of the samples used for this study. Pf-HRP 2 antibody was conjugated to freshly prepared colloidal gold of particle size 40nm. The conjugation process was blocked with bovine serum albumin (BSA) and the conjugate itself preserved by 1% glycerol and 0.01% sodium azide. The parasite count was titrated against the Pf-HRP 2gold conjugate and was analyzed under the light microscope with a fluorescent filter. Reactivity and specificity of Pf-HRP 2 gold conjugate was found to be highly specific and gave direct identification of the erythrocytes infected with the parasite. A good contrast was also obtained between uninfected erythrocytes, parasite and the infected erythrocytes
The Cytoarchitectural alterations in the neocortex of Wistar rats: Effects of aqueous tobacco (Nicotiana tabacum) leaves extract exposure
This study investigated the effects of corresponding 11.7 mg/kg body weight and 5.8 mg/kg body weight/day of the tobacco leaves aqueous extract for a period of 20 days on the functions of rats’ brain after extract administration. Nicotiana tabacum is the scientific name of the tobacco plant grown in several countries of the world. It has been used in variables ways such as smoking, snuffing, even chewing, etc. 24 young rats of both sexes were used. They were divided into 3 groups, A, B, C of 8 rats each (Female (n = 4) and male (n = 4)). Group A were given 11.7 mg of the extract per kg body weight, group B 5.8 mg of the extract per kg body weight in 0.5 ml of distilled water per day throughout the 20 experimental days while group C were given equal volume (0.5 ml) of distilled water as well. The rats were sacrificed at day 21 by cervical dislocation and the brains were excised and fixed in formol calcium for 4 days and processed using Haematoxylin and Eosin staining method and Cresyl Fast Violet (CFV) staining technique. There was a statistical significant decrease in the body weight, brain weight and relative brain weight between groups A and B compared to the control group (p < 0.05). There was enlargement of the somata in the group A administered with 11.7 mg/kg B.Wt per day of the extract while those in group B appeared more spindle compared to those cells in group C. Also, the non – homogenous appearance of myelinated neocortex of the neuropil appear clearly in the treated groups compared to control (Figure 3). Therefore, the results suggested that the consumption of the aqueous extract of N. tabacum leaves may alter the normal functions of the brain which may lead to brain dysfunction, despite its “pleasant” effects and also help in reduction in weight gain
Demilitarisation Nigeria and South Africa compared
In sub-Saharan African countries that have made democratic transition from military
rule and military-backed authoritarian regimes, state elites have embarked upon
strategies aimed at demilitarising the new democratic political process. Demilitarisation
of the state and politics has become an imperative because it is decisive for
consolidating democratic politics and for ensuring improvements in public safety and
security. Yet the process of such demilitarisation in these countries has often generated
a paradox, whereby the reduction of the political influence of state institutions of
violence has been associatedw ith rising civil militarism and the prevalenceo f organised
violence in the wider society.
In these circumstances, taking cognisance of the dangers of civil militarism and other
forms of private violence is a priority for designing and implementing demilitarisation
strategies and other security reforms in post-authoritarian African states. Reformminded
political elites and external supporters need to be sensitive to these dangers or
risk perpetuating the shell of electoral democracy that cannot deliver the goal of human
security in the region. This dissertation explored how the current approach to
demilitarisation is related to the problem of civil militarism by examining the case
studies of Nigeria and South Africa. It explains that given the condition of the state in
Africa, demilitarisation of politics after transition from military or military-backed
authoritarianism contributes to the emergence of civil militarism. Based on this finding,
it argues for a comprehensive approach to demilitarisation as a strategy that caters to
both state and societal violence in order to mitigate the risks of civil militarism in the
process
