Polyphenol-rich fraction of Alchornea cordifolia leaf ameliorates arsenite-induced infertility in male rats.

Alchornea cordifolia is used traditionally for the treatment of infertility and venereal diseases. Thirty rats were randomly divided into five groups of six rats each: Group 1 (distilled water), group 2 (7 mg/kg sodium arsenite), group 3 (7 mg/kg sodium arsenite and 100 µg/kg polyphenol-rich fraction 1 of A. cordifolia), group 4 (7 mg/kg sodium arsenite + 100 µg/kg polyphenol-rich fraction 2) and group 5 (7 mg/kg sodium arsenite + α-tocopherol). The experiment lasted 30 consecutive days. Biochemical markers of oxidative stress and antioxidants, male reproductive hormones, spermatozoa function tests, histopathology, immunoreactivity of androgen receptor binding protein (ARBP) and anti-apoptotic B-cell lymphoma-2 protein expressions were estimated. Data were analysed using descriptive statistics and ANOVA at p < .05. Treatment with AF1 significantly decreased markers of oxidative stress, but increased the systemic antioxidants, testosterone, FSH, spermatozoa count and motility. Histopathological lesions of necrosis and germinal epithelial sloughing observed in sodium arsenite group were absent in sodium arsenite + 100 µg/kg polyphenol-rich fraction 1 group. Expressions of androgen receptor binding protein and anti-apoptotic B-cell lymphoma-2 were highest in sodium arsenite + 100 µg/kg polyphenol-rich fraction 1 group. In conclusion, the polyphenol-rich fraction of A. cordifolia is protective against sodium arsenite-induced infertility in male rats through the inhibition of oxidative and apoptotic mechanisms.

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.

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.

Modulatory effects of melatonin and vitamin  C on oxidative stress-mediated haemolytic anaemia and associated cardiovascular dysfunctions in rats.

Background Phenylhydrazine (PHE) in experimental animal models has been widely reported to cause haemolytic anaemia, via the induction of oxidative stress and thus causing deleterious cardiovascular complications. Hence, this study was designed to evaluate the possible modulatory role of melatonin (MLT) or vitamin C when co-administered with PHE. Methods Anaemia was established with PHE administration. MLT or vitamin C was co-administered with PHE. Haematological parameters, markers of oxidative stress, enzymic and non-enzymic antioxidants, blood pressure and electrocardiograms were assessed. Results PHE administration led to a significant (p<0.05) increase in malondialdehyde (MDA), and hydrogen peroxide (H2O2) generated in cardiac, renal and red blood cell (RBC) lysates. PHE also significantly reduced the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and reduced glutathione (GSH) contents, respectively. The RBC counts, haemoglobin (Hb) concentration and packed cell volume (PCV) were also significantly reduced following the administration of PHE. Furthermore, the systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial blood pressure (MABP) increased significantly in rats administered PHE alone. Similarly, PHE administration led to a significant drop in heart rate but prolonged QRS, QT and QTc interval. Pathology of the heart and kidney was also observed in PHE treated group. However, treatment with MLT and vitamin C improved enzymic and non-enzymic antioxidant system together with the restoration of SBP, DBP and MABP to near normal. The architectural anarchy observed in the heart and kidney of PHE administered rats was reversed to some extent. Conclusions Hence, MLT and vitamin C could be employed as therapeutic targets in various cardiovascular diseases and its complications.

Phytochemical screening and toxicity studies on the methanol extract of the seeds of moringa oleifera.

The seeds of Moringa oleifera were collected, air-dried, pulverized, and subjected to cold extraction with methanol. The methanol extract was screened phytochemically for its chemical components and used for acute and sub-acute toxicity studies in rats. The phytochemical screening revealed the presence of saponins, tannins, terpenes, alkaloids, flavonoids, carbohydrates, and cardiac glycosides but the absence of anthraquinones. Although signs of acute toxicity were observed at a dose of 4,000 mg kg-1 in the acute toxicity test, and mortality was recorded at 5,000 mg kg-1, no adverse effect was observed at concentrations lower than 3,000 mg kg-1. The median lethal dose of the extract in rat was 3,873 mg kg-1. Sub-acute administration of the seed extract caused significant (p<0.05) increase in the levels of alanine and aspartate transferases (ALT and AST), and significant (p<0.05) decrease in weight of experimental rats, at 1,600 mg kg-1. The study concludes that the extract of seeds of M. oleifera is safe both for medicinal and nutritional uses.