Vanadium administration ameliorates cortical structural and functional changes in juvenile hydrocephalic mice.

Vanadium is a prevalent neurotoxic transition metal with therapeutic potentials in some neurological conditions. Hydrocephalus poses a major clinical burden in neurological practice in Africa. Its primary treatment (shunting) has complications, including infection and blockage; alternative drug-based therapies are therefore necessary. This study investigates the function and cytoarchitecture of motor and cerebellar cortices in juvenile hydrocephalic mice following treatment with varying doses of vanadium. Fifty juvenile mice were allocated into five groups (n = 10 each): controls, hydrocephalus-only, low- (0.15 mg/kg), moderate- (0.3 mg/kg), and high- (3.0 mg/kg) dose vanadium groups. Hydrocephalus was induced by the intracisternal injection of kaolin and sodium metavanadate administered by intraperitoneal injection 72hourly for 28 days. Neurobehavioral tests: open field, hanging wire, and pole tests, were carried out to assess locomotion, muscular strength, and motor coordination, respectively. The cerebral motor and the cerebellar cortices were processed for cresyl violet staining and immunohistochemistry for neurons (NeuN) and astrocytes (glial fibrillary acidic protein). Hydrocephalic mice exhibited body weight loss and behavioral deficits. Horizontal and vertical movements and latency to fall from hanging wire were significantly reduced, while latency to turn and descend the pole were prolonged in hydrocephalic mice, suggesting impaired motor ability; this was improved in vanadium-treated mice. Increased neuronal count, pyknotic cells, neurodegeneration and reactive astrogliosis were observed in the hydrocephalic mice. These were mostly mitigated in the vanadium-treated mice, except in the high-dose group where astrogliosis persisted. These results demonstrate a neuroprotective potential of vanadium administration in hydrocephalus. The molecular basis of these effects needs further exploration.

Neuropathological profile of the African Giant Rat brain (Cricetomys gambianus) after natural exposure to heavy metal environmental pollution in the Nigerian Niger Delta.

Pollution by heavy metals is a threat to public health because of the adverse effects on multiple organ systems including the brain. Here, we used the African giant rat (AGR) as a novel sentinel host to assess the effect of heavy metal accumulation and consequential neuropathology upon the brain. For this study, AGR were collected from distinct geographical regions of Nigeria: the rain forest region of south-west Nigeria (Ibadan), the central north of Nigeria (Abuja), and in oil-polluted areas of south Nigeria (Port-Harcourt). We found that zinc, copper, and iron were the major heavy metals that accumulated in the brain and serum of sentinel AGR, with the level of iron highest in animals from Port-Harcourt and least in animals from Abuja. Brain pathology, determined by immunohistochemistry markers of inflammation and oxidative stress, was most severe in animals from Port Harcourt followed by those from Abuja and those from Ibadan were the least affected. The brain pathologies were characterized by elevated brain advanced oxidation protein product (AOPP) levels, neuronal depletion in the prefrontal cortex, severe reactive astrogliosis in the hippocampus and cerebellar white matter, demyelination in the subcortical white matter and cerebellar white matter, and tauopathies. Selective vulnerabilities of different brain regions to heavy metal pollution in the AGR collected from the different regions of the country were evident. In conclusion, we propose that neuropathologies associated with redox dyshomeostasis because of environmental pollution may be localized and contextual, even in a heavily polluted environment. This novel study also highlights African giant rats as suitable epidemiological sentinels for use in ecotoxicological studies.

GluN2A and GluN2B N-Methyl-D-Aspartate Receptor (NMDARs) Subunits: Their Roles and Therapeutic Antagonists in Neurological Diseases.

N-methyl-D-aspartate receptors (NMDARs) are ion channels that respond to the neurotransmitter glutamate, playing a crucial role in the permeability of calcium ions and excitatory neurotransmission in the central nervous system (CNS). Composed of various subunits, NMDARs are predominantly formed by two obligatory GluN1 subunits (with eight splice variants) along with regulatory subunits GluN2 (GluN2A-2D) and GluN3 (GluN3A-B). They are widely distributed throughout the CNS and are involved in essential functions such as synaptic transmission, learning, memory, plasticity, and excitotoxicity. The presence of GluN2A and GluN2B subunits is particularly important for cognitive processes and has been strongly implicated in neurodegenerative diseases like Parkinson's disease and Alzheimer's disease. Understanding the roles of GluN2A and GluN2B NMDARs in neuropathologies provides valuable insights into the underlying causes and complexities of major nervous system disorders. This knowledge is vital for the development of selective antagonists targeting GluN2A and GluN2B subunits using pharmacological and molecular methods. Such antagonists represent a promising class of NMDA receptor inhibitors that have the potential to be developed into neuroprotective drugs with optimal therapeutic profiles.

Vanadium improves memory and spatial learning and protects the pyramidal cells of the hippocampus in juvenile hydrocephalic mice.

Background: Hydrocephalus is a neurological condition known to cause learning and memory disabilities due to its damaging effect on the hippocampal neurons, especially pyramidal neurons. Vanadium at low doses has been observed to improve learning and memory abilities in neurological disorders but it is uncertain whether such protection will be provided in hydrocephalus. We investigated the morphology of hippocampal pyramidal neurons and neurobehavior in vanadium-treated and control juvenile hydrocephalic mice. Methods: Hydrocephalus was induced by intra-cisternal injection of sterile-kaolin into juvenile mice which were then allocated into 4 groups of 10 pups each, with one group serving as an untreated hydrocephalic control while others were treated with 0.15, 0.3 and 3 mg/kg i.p of vanadium compound respectively, starting 7 days post-induction for 28 days. Non-hydrocephalic sham controls (n = 10) were sham operated without any treatment. Mice were weighed before dosing and sacrifice. Y-maze, Morris Water Maze and Novel Object Recognition tests were carried out before the sacrifice, the brains harvested, and processed for Cresyl Violet and immunohistochemistry for neurons (NeuN) and astrocytes (GFAP). The pyramidal neurons of the CA1 and CA3 regions of the hippocampus were assessed qualitatively and quantitatively. Data were analyzed using GraphPad prism 8. Results: Escape latencies of vanadium-treated groups were significantly shorter (45.30 ± 26.30 s, 46.50 ± 26.35 s, 42.99 ± 18.44 s) than untreated group (62.06 ± 24.02 s) suggesting improvements in learning abilities. Time spent in the correct quadrant was significantly shorter in the untreated group (21.19 ± 4.15 s) compared to control (34.15 ± 9.44 s) and 3 mg/kg vanadium-treated group (34.35 ± 9.74 s). Recognition index and mean % alternation were lowest in untreated group (p = 0.0431, p=0.0158) suggesting memory impairments, with insignificant improvements in vanadium-treated groups. NeuN immuno-stained CA1 revealed loss of apical dendrites of the pyramidal cells in untreated hydrocephalus group relative to control and a gradual reversal attempt in the vanadium-treated groups. Astrocytic activation (GFAP stain) in the untreated hydrocephalus group were attenuated in the vanadium-treated groups under the GFAP stain. Pyknotic index in CA1 pyramidal layer of untreated (18.82 ± 2.59) and 0.15mg/kg vanadium-treated groups (18.14 ± 5.92) were significantly higher than control (11.11 ± 0.93; p = 0.0205, p = 0.0373) while there was no significant difference in CA3 pyknotic index across all groups. Conclusion: Our results suggest that vanadium has a dose-dependent protective effect on the pyramidal cells of the hippocampus and on memory and spatial learning functions in juvenile hydrocephalic mice.

Permanent Tooth Eruption Patterns in Nigerian Local Pigs.

Pigs are diphyodonts with heterodont dentition and have been used in studies involving teeth and jawbone regeneration, and dental implants. Patterns of tooth eruption are used to age animals and determine the effects of environmental and genetic influences on occurrence of variations. As with other species, variations exist in the tooth eruption pattern in pigs. The aim of this study was to determine the permanent teeth eruption patterns of Nigerian local pigs. Twenty-six healthy pigs were observed throughout the study period. Pigs were firmly held in dorsal or lateral recumbency and their mouths gently held open to visually examine all quadrants of the dental arches (right and left maxillary, right and left mandibular). Observations were recorded from 16 weeks of age, until the last permanent tooth erupted. Results obtained from the study showed that males had lower mean values for eruption time (54%) of examined teeth in comparison to females. The mean values of eruption time for the maxillary third incisor, the mandibular and maxillary canines, and the mandibular fourth premolar teeth were statistically significant in the males (P = .0017, P = .0088, P = .0002 and P = .0244, respectively). Sixty-nine percent of the adult pigs did not have eruption of the mandibular first premolar, while polydontia was observed in the maxillary and mandibular incisors. These results show that intra-breed and inter-breed variations exist in the dental eruption pattern in pigs. The data obtained from this study can be used for comparative dental studies and can aid further research on the developmental anatomy of Nigerian local pigs.

Leaf extract of Anacardium occidentale ameliorates biomarkers of neuroinflammation, memory loss, and neurobehavioral deficit in N(ω)-nitro-L-arginine methyl ester (L-NAME) treated rats.

PURPOSE: Anacardium occidentale commonly known as Cashew is a plant that is widely used in African traditional medicine. It is endowed with phytochemical constituents that are responsible for its medicinal properties. METHODS: Twenty-five male Wistar rats were grouped as follows: Control (Group A), Group B (L-NAME 40 mg/kg), Group C (100 mg/kg Anacardium occidentale extract plus 40 mg/kg L-NAME), Group D (200 mg/kg extract plus 40 mg/kg L-NAME) and Group E (10 mg/kg of Lisinopril plus 40 mg/kg L-NAME). The animals were treated with oral administration of either the extracts or Lisnopril daily for 4 weeks. Neuro-behavioural tests such as the Morris Water Maze and Hanging Wire Grip tests were carried out to evaluate memory/spatial learning and muscular strength, respectively. Makers of oxidative stress, antioxidant enzymes and immunohistochemical staining of Glial Fibrillary Acidic Protein and Ionised Calcium Binding Adaptor molecule 1 were assessed. RESULTS: L-NAME administration caused significant increases in biomarkers of oxidative stress, decreased antioxidant status, acetylcholinesterase activity, altered neuro-behavioural changes, astrocytosis, and microgliosis. However, Anacardium occidentale reversed exaggerated oxidative stress biomarkers and improved neuro-behavioural changes. CONCLUSIONS: Combining all, Anacardium occidentale enhanced brain antioxidant defence status, improved memory and muscular strength, thus, suggesting the neuroprotective properties of Anacardium occidentale.

Dental Disorders in Wild and Domestic Pigs (Sus Scrofa): A Review.

Teeth in the mouth of vertebrates represent the modified descendants of bony dermal plates of ancestral fishes. Dental disorders, which are deviations of dental tissues origins, are derived from any or all of the dental tissues; enamel, dentin or cementum, and include dental abnormalities and diseases. These disorders can be influenced by genetic or environmental factors, or an interplay of both factors. This article reviews disorders that have been reported in both wild and domestic pigs and the frequency of occurrence of these conditions.

Astrocytes and Microglia in Stress-Induced Neuroinflammation: The African Perspective.

Background: Africa is laden with a youthful population, vast mineral resources and rich fauna. However, decades of unfortunate historical, sociocultural and leadership challenges make the continent a hotspot for poverty, indoor and outdoor pollutants with attendant stress factors such as violence, malnutrition, infectious outbreaks and psychological perturbations. The burden of these stressors initiate neuroinflammatory responses but the pattern and mechanisms of glial activation in these scenarios are yet to be properly elucidated. Africa is therefore most vulnerable to neurological stressors when placed against a backdrop of demographics that favor explosive childbearing, a vast population of unemployed youths making up a projected 42% of global youth population by 2030, repressive sociocultural policies towards women, poor access to healthcare, malnutrition, rapid urbanization, climate change and pollution. Early life stress, whether physical or psychological, induces neuroinflammatory response in developing nervous system and consequently leads to the emergence of mental health problems during adulthood. Brain inflammatory response is driven largely by inflammatory mediators released by glial cells; namely astrocytes and microglia. These inflammatory mediators alter the developmental trajectory of fetal and neonatal brain and results in long-lasting maladaptive behaviors and cognitive deficits. This review seeks to highlight the patterns and mechanisms of stressors such as poverty, developmental stress, environmental pollutions as well as malnutrition stress on astrocytes and microglia in neuroinflammation within the African context.

Reproductive Hormones Imbalance, Germ Cell Apoptosis, Abnormal Sperm Morphophenotypes and Ultrastructural Changes in Testis of African Giant Rats (Cricetomys gambianus) Exposed to Sodium Metavanadate Intoxication.

Environmental exposure to vanadium has been on the increase in recent time. This metal is a known toxicant. The current study was conducted to investigate the reproductive toxicity of sodium metavanadate (SMV) in male African giant rats. Administration of SMV was done intraperitoneally daily for 14 consecutive days at a dosage of 3 mg/kg body weight. Sterile water was administered to the control group. Serum reproductive hormones, sperm reserve and quality as well as testicular ultrastructural changes following SMV treatment were analysed. Results showed SMV-exposed AGR group had statistically decreased concentrations of testosterone (4.7 ng/ml), FSH (3.4 IU/L) and LH (3.8 IU/L). Also, SMV-treated group had statistically decreased sperm motility and mass activity with increased percentage of abnormal morphophenotypes of spermatozoa and upregulation of P53 immunopositive cells. Ultrastructural study revealed vacuolation of germ and Sertoli cells cytoplasm and nucleus, and mitochondrial swelling and vacuolations were also observed. There was severe disintegration of the seminiferous tubules, atrophy and degeneration of myeloid cells and apoptosis of the Leydig, Sertoli and germ cells. In conclusion, intraperitoneal SMV exposure exerts severe adverse effects on some serum reproductive hormones, reduction in the sperm reserve and quality, apoptosis and degenerative changes of the Leydig, Sertoli and germ cells which can lead to infertility.

Neuroecotoxicology: Effects of environmental heavy metal exposure on the brain of African giant rats and the contribution of vanadium to the neuropathology.

Increased exploitation of minerals has led to pollution of confined environments as documented in Nigeria Niger Delta. Information on the effects on brain of such exposure is limited. Due to its exploratory activities, the African giant rat (Cricetomys gambianus) (AGR) provides a unique model for neuroecotoxicological research to determine levels of animal and human exposure to different pollutants. This study aims to unravel neuropathological features of AGR sampled from three agro-ecological zones of Nigeria. Fifteen AGR were sampled according to previously determined data on heavy metal exposure: high vanadium, high lead, and low metals. Eighteen AGR were collected from low metal zone and divided into two groups. Control group received vehicle while SMV exposed group received 3 mg/kg sodium metavanadate (SMV) intraperitoneally for 14days. Brain immunohistochemical analyses were conducted, and ultrastructural changes were studied in experimentally exposed group. Results showed significant loss of tyrosin hydroxylase, parvalbumin, orexin-A and melanin concentration hormone containing neuronal populations in brains obtained from high vanadium and high lead zones and in experimentally intoxicated SMV groups. Similarly, significant decrease numbers of dendritic arborations; extracellular matrix density, perineuronal nets; astrocytes and microglia activations are documented in same groups. Ultrastructural studies revealed mass denudation, cilia loss, disintegration of ependymal layer and intense destructions of myelin sheaths in SMV exposed group. These are the first "neuroecotoxicological" findings in distinct neuronal cells. The implications of these findings are highly relevant for human population living in these areas, not only in Nigeria but also in similarly polluted areas elsewhere in the world.

Molecular detection of dugbe orthonairovirus in cattle and their infesting ticks (Amblyomma and Rhipicephalus (Boophilus)) in Nigeria.

Dugbe orthonairovirus (DUGV), a tick-borne zoonotic arbovirus, was first isolated in 1964 in Nigeria. For over four decades, no active surveillance was conducted to monitor the spread and genetic variation of DUGV. This study detected and genetically characterized DUGV circulating in cattle and their infesting ticks (Amblyomma and Rhipicephalus (Boophilus)) in Kwara State, North-Central Nigeria. Blood and or ticks were collected from 1051 cattle at 31 sampling sites (abattoirs and farms) across 10 local government areas of the State. DUGV detection was carried out by RT-qPCR, and positive samples sequenced and phylogenetically analysed. A total of 11824 ticks, mostly A. variegatum (36.0%) and R. (B.) microplus (63.9%), were obtained with mean tick burden of 12 ticks/cattle. Thirty-four (32 A. variegatum and two R. (B.) microplus) of 4644 examined ticks were DUGV-positive, whereas all of the cattle sera tested negative for DUGV genome. Whole genome sequence (S, M and L segments) and phylogenetic analyses indicate that the positive samples shared up to 99.88% nucleotide identity with and clustered around the Nigerian DUGV prototype strain IbAr 1792. Hence, DUGV with high similarity to the previously characterised strain has been detected in Nigeria. To our knowledge, this is the first report of DUGV in North-Central Nigeria and the most recent information after its last surveillance in 1974.

Ameliorative effects of the aqueous extract of Khaya anthotheca (Welw.) C.DC (Meliaceae) in vanadium induced anxiety, memory loss and pathologies in the brain and ovary of mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Ethnobotanical enquiries have revealed that Khaya anthotheca (Welw.) C.DC (Meliaceae) has anxiolytic properties and is used to alleviate vaginal dryness in postmenopausal women in Cameroon. The aim of this study was to evaluate the ameliorative effects of the aqueous extract of K. anthotheca in vanadium induced anxiety, memory loss and pathologies in the brain and ovary of mice. MATERIAL AND METHODS: Forty neonatal female mice were used in this study. All animals received vanadium (3 mg/kg BW/72 h, by lactation and i.p.) for 20 weeks except the Control group. At 16 weeks old, mice were divided into 5 groups (n = 8): Control group received distilled water; V-group received vanadium (V) (3 mg/kg BW every 72 h i.p.), V + Vit E group received vitamin E (500 mg/kg BW/72 h) and vanadium (V) (3 mg/kg BW/72 h i.p, simultaneously). V + KA 125 and V + KA 250 groups received K. anthotheca extract at the doses of 125 and 250 mg/kg BW/day respectively and vanadium (V) (3 mg/kg BW/72 h i.p, simultaneously).The treatment was done per os at 10 mL/kg of volume of administration for 4 weeks. To evalute anxiolytic effects and spatial working memory improved by the extract in mice, the elevated open space test and Y maze test were used respectively. After sacrifice, brains were harvested and pathologies were assessed using cresyl violet stainning and immunohistochemistry (GFAP, Iba-1 and MBP), while pathologies in the ovaries were assessed using immunohistochemistry (Collagen type 1) and H&E stainning. RESULTS: Results in the three sessions of elevated open space test showed that vanadium exposure resulted in a significant (p < 0.05; p < 0.01) increase of the latency of first entry in the slopes and a significant (p < 0.05; p < 0.01; p < 0.001) decrease of the time spent and number of entries in the slopes however, Khaya anthotheca treatment induced a significant (p < 0.05; p < 0.01) decrease of the latency of first entry in the slopes and a significant (p < 0.05; p < 0.01) increase of the time spent and number of entries in the slopes. In the Y maze test, vanadium exposure resulted in a significant decrease (p < 0.01) in the percentage of correct alternation, K. anthotheca extract at the dose of 250 mg/kg BW however induced a significant (p < 0.05) increase of this percentage of correct spontaneous alternation. In the brain, degeneration induced by vanadium exposure was marked by an increase of GFAP-immunoreactive cells, microgliosis and demyelination. The treatment with Khaya anthotheca extract at the dose of 250 mg/kg BW resulted in the preservation of cellular integrity in the same anatomical regions with reduced astroglial and microglial activation and prevented demyelination. In addition, vanadium exposure decreased Collagen type 1 expression in the ovaries and induced a deterioration of tertiary follicle. Khaya anthotheca treatment at the dose of 250 mg/kg BW induced an increase of expression of Collagen type 1 and alleviated deterioration of the microarchitecture of tertiary follicle induced by vanadium. CONCLUSION: These effects induced by K. anthotheca extract could justify the traditional use of this plant in Cameroonian traditional medicine to manage anxiety. Therefore, to minimise vanadium induced toxicity, the plant should be given more emphasis as a candidate in developing a modern phytodrug.

Essential Metals in the Brain and the Application of Laser Ablation-Inductively Coupled Plasma-Mass Spectrometry for their Detection.

Metals are natural component of the ecosystem present throughout the layers of atmosphere; their abundant expression in the brain indicates their importance in the central nervous system (CNS). Within the brain tissue, their distribution is highly compartmentalized, the pattern of which is determined by their primary roles. Bio-imaging of the brain to reveal spatial distribution of metals within specific regions has provided a unique understanding of brain biochemistry and architecture, linking both the structures and the functions through several metal mediated activities. Bioavailability of essential trace metal is needed for normal brain function. However, disrupted metal homeostasis can influence several biochemical pathways in different fields of metabolism and cause characteristic neurological disorders with a typical disease process usually linked with aberrant metal accumulations. In this review we give a brief overview of roles of key essential metals (Iron, Copper and Zinc) including their molecular mechanisms and bio-distribution in the brain as well as their possible involvement in the pathogenesis of related neurodegenerative diseases. In addition, we also reviewed recent applications of Laser Ablation Inductively Couple Plasma Mass Spectrophotometry (LA-ICP-MS) in the detection of both toxic and essential metal dyshomeostasis in neuroscience research and other related brain diseases.

Attenuation of ischemia-reperfusion-induced gastric ulcer by low-dose vanadium in male Wistar rats.

AIM: Vanadium, a trace element found in food and water sources has been previous reported to attenuate ulcer formation without much insight into its mechanism of action. This study highlights the mechanism by which vanadium exhibits its gastro-protective activity. MAIN METHODS: Eighty male Wistar rats (80-100 g) were randomized into 8 equal groups. Groups 1 (control) and 2 (Ulcerated control) received water only, groups 3-8 received vanadium at 5, 10, 25, 50, 100 and 200 ppm respectively in their drinking water for ten weeks. Gastric ulcer was thereafter induced in groups (2-8) via ischaemia-reperfusion (IR) technique. The stomachs were excised for macroscopic examination, evaluation of mucous content, oxidative stress markers, hydrogen/potassium (H+/K+) and calcium (Ca++) ATPases activities plus expression of induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Vanadium at low doses inhibited IR induced gastric ulcer by 62.62% (10 ppm), 54.80% (25 ppm) and 43.50% (50 ppm). KEY FINDINGS: Low dose vanadium increased mucous content, superoxide dismutase, catalase, glutathione activities and nitrite concentrations compared to ulcerated control group. The observed increase in malondialdehyde, Ca++ and H+/K+ ATPase activities, iNOS and COX-2 expression following IR were significantly reduced by pretreatment with vanadium. SIGNIFICANCE: This study demonstrated that vanadium at low doses exhibit gastro-protective activities on IR induced gastric ulcer in rat model by inhibiting proton pump activities and decreasing expressions of iNOS and COX-2, thereby giving more insight into the protective action of vanadium.

Biochemical and ultrastructural changes in kidney and liver of African Giant Rats (Cricetomysgambianus, Waterhouse, 1840) exposed to intraperitoneal sodium metavanadate (vanadium) intoxication.

We studied the hepatic and renal impact of sodium metavanadate (SMV) exposure in African giant rats (AGR). Twelve male AGR were used and divided into two groups. The control group received sterile water while the SMV-exposed group received 3 mg/kg SMV intraperitoneally for 14 days. SMV exposed AGR groups showed significantly decreased activities of serum AST, ALT, ALP and creatinine concentration but increased blood urea nitrogen (BUN), albumin and globulin concentrations. Kidney ultrastructure examination revealed atrophy of the glomerular tuft, loss of podocytes, distortions of the endothelium and glomerular basement membrane. The liver sinusoids fenestration phenotypes were abnormal. Hepatocytes exhibited hypertrophy with uneven, crenated and dentate nuclei. SMV exposure induced activation of monocytes, as well as Kupffer and fibrous cells. Alterations in glomerular podocytes and cell-cell and cell matrix contact and inflammatory liver fibrosis are key events in progressive glomerular failure and hepatic damage due to SMV intoxication.

A study of scientific publications on the greater cane rat (Thryonomys swinderianus, Temminck 1827).

BACKGROUND: The greater cane rat (GCR), reputed to be African's second largest rodent, is a precocial hystricomorph with an uncommon phenotype and life history. Scientific and socio-economic interests in the GCR have led to heightened research efforts targeted towards a better understanding of its biology and exploration of its economic and translational usefulness. METHODS: Records of all online scientific publications on the GCR from Google, Google Scholar, PubMed, science.gov, Ebscohost and Worldwide science, with the exception of research theses, proceedings, unpublished projects and abstracts, were collated and analyzed using descriptive statistics. RESULTS: A total of 146 published scholarly articles spanning about six decades were retrieved, with 98% of the GCR publications originating from African countries. Nigeria boasts the highest number of publications (58.22%) followed by Ghana (21.23%) and South Africa (5.48%) while Senegal contributed the least (0.69%). Publications were sorted into ten field categories. The field with the highest number of articles (41.78%) was animal breeding and management recording, closely followed by anatomy (37.67%). Lesser contributions were made by parasitology (5.48%), biochemistry/hematology (4.8%), pharmacology/toxicology (4.11%), pathology (2.06%), and surgery/anesthesia and physiology (1.37% apiece). The fields with fewest contributions were microbiology and developmental biology (0.69% each). CONCLUSION: This study chronicles the spectrum of knowledge available on the GCR, highlighting the knowledge gap that still exists in various fields in order to provide advocacy for new frontiers in research efforts on this rodent. We suggest the need for a clearly defined and well integrated national/regional policy aimed at establishing Africa's foremost micro-livestock rodent, the greater cane rat, on the world's scientific radar.

Βeta-sitosterol enhances motor coordination, attenuates memory loss and demyelination in a vanadium-induced model of experimental neurotoxicity.

Environmental discharge of vanadium causes cognitive and behavioral impairments in humans and animals via production of reactive oxygen species leading to lipid peroxidation and alteration in antioxidant defence system. The current study was carried out to investigate the cognitive-enhancing ability of ß-sitosterol in vanadium-induced neurotoxicity. Forty eight mice were randomly assigned into 4 groups (A-D) with the following treatments: group A; distilled water, B; α-tocopherol + sodium metavanadate (NaO3V), C; ß-sitosterol + NaO3V and D; only NaO3V. NaO3V was administered intraperitoneally while other treatments were administered through gavage for 7 consecutive days. Neurobehavioral parameters measuring cognition, locomotion, anxiety and grip strength were evaluated at day 8. Following sacrifice, brain levels of catalase, superoxide dismutase, glutathione, malonaldehyde (MDA) and hydrogen peroxide (H2O2) were measured. Immunohistochemical expression of Myelin Basic Protein (MBP) in the brain was also investigated. The results showed that deficits in spatial learning, locomotor efficiency, and motor coordination, induced by acute vanadium neurotoxicity were mitigated by beta-sitosterol. Significantly (α ≤ 0.05) decreased in vivo antioxidant enzyme activities, increased brain levels of MDA and H2O2, structural damage to myelin sheaths and decreased expression of MBP were also observed in the NaO3V group (D), however, co-administration of ß-sitosterol reduced these pathologic features. It is concluded that ß-sitosterol alleviates vanadium-induced neurotoxicity by enhancing cognition and improving motor co-ordination via its antioxidant and myelo-protective activities.

Intraperitoneal sodium metavanadate exposure induced severe clinicopathological alterations, hepato-renal toxicity and cytogenotoxicity in African giant rats (Cricetomys gambianus, Waterhouse, 1840).

Pollution of environment due to increased exploitation of minerals has been on the rise, and vanadium, a metal in the first transition series essential for mammalian existence, is a major component of air pollution. This study investigated the clinico-pathological, hepato-renal toxicity, and cytogenotoxicity of intraperitoneal exposure of African giant rats (AGRs), a proposed model for ecotoxicological research to sodium metavanadate. A total of 27 adult male African giant rats weighing 975 ± 54.10 g were distributed into two major groups: sodium metavanadate (SMV) treated and control. They were observed daily for clinical signs of toxicity. Four rats from each group were randomly collected and sacrificed after 3, 7, and 14 days of SMV treatment. Liver, kidney, and bone marrow were analyzed for histopathology and micronucleated normochromated and polychromated erythrocytes (MNNCE and MNPCE), respectively. Clinical signs in treated AGR include sluggish and weak movements, un-groomed fur, and labored breathing. Histology of the kidney revealed severe glomerular atrophy, tubular ectasia, and vacuolar degeneration of tubular epithelium, while liver histology showed sinusoidal congestion and severe hepatocellular necrosis after 14 days SMV exposure. Also, MNNCE and MNPCE significantly increased with a decrease in PCE/NCE ratio in SMV-treated AGR, suggestive of alternations in bone marrow cell proliferation. Hence, SMV treatment to AGR resulted to severe clinicopathologic alterations, kidney, and liver dysfunction and cytogenotoxicity evident by somatic mutation induction which could be severe with prolonged exposure. This suggests African giant rat as an ecotoxicological model to measure major health risks to animals and human populations in highly polluted environment.

Sodium metavanadate induced cognitive decline, behavioral impairments, oxidative stress and down regulation of myelin basic protein in mice hippocampus: Ameliorative roles of ß-spinasterol, and stigmasterol.

INTRODUCTION: Exposures to toxic levels of vanadium and soluble vanadium compounds cause behavioral impairments and neurodegeneration via free radical production. Consequently, natural antioxidant sources have been explored for effective and cheap remedy following toxicity. Grewia carpinifolia has been shown to improve behavioral impairments in vanadium-induced neurotoxicity, however, the active compounds implicated remains unknown. Therefore, this study was conducted to investigate ameliorative effects of bioactive compounds from G. carpinifolia on memory and behavioral impairments in vanadium-induced neurotoxicity. METHODS: Sixty BALB/c mice were equally divided into five groups (A-E). A (control); administered distilled water, B (standard); administered α-tocopherol (500 mg/kg) every 72 hr orally with daily dose of sodium metavanadate (3 mg/kg) intraperitoneally, test groups C, and D; received single oral dose of 100 µg ß-spinasterol or stigmasterol (bioactive compounds from G. carpinifolia), respectively, along with sodium metavanadate and the model group E, received sodium metavanadate only for seven consecutive days. Memory, locomotion and muscular strength were accessed using Morris water maze, Open field and hanging wire tests. In vivo antioxidant and neuroprotective activities were evaluated by measuring catalase, superoxide dismutase, MDA, H2 O2 , and myelin basic protein (MBP) expression in the hippocampus. RESULTS: In Morris water maze, stigmasterol significantly (p ≤ 0.05) decreased escape latency and increased swimming time in target quadrant (28.01 ± 0.02; 98.24 ± 17.38 s), respectively, better than α-tocopherol (52.43 ± 13.25; 80.32 ± 15.21) and ß-spinasterol (42.09 ± 14.27; 70.91 ± 19.24) in sodium metavanadate-induced memory loss (112.31 ± 9.35; 42.35 ± 11.05). ß-Spinasterol and stigmasterol significantly increased exploration and latency in open field and hanging wire tests respectively. Stigmasterol also increased activities of antioxidant enzymes, decreased oxidative stress markers and lipid peroxidation in mice hippocampal homogenates, and increased MBP expression. CONCLUSIONS: The findings of this study indicate a potential for stigmasterol, a bioactive compound from G. carpinifolia in improving cognitive decline, motor coordination, and ameliorating oxidative stress in vanadium-induced neurotoxicity.