Reno-Hepatoprotective and Antidiabetic Properties of Methanol Leaf Extract of Laportea Aestuans in Wistar Rats.

Toxicities due to exposure to arsenic-contaminated water and the occurrence of diabetes mellitus are major health concerns. Treatment of these concerns using therapeutic measures have recorded limited success. Traditionally, Laportea aestuans (LA) has been used in managing various diseases. Hence, we investigated the reno-hepatoprotective/antidiabetic potentials of methanol leaf extract of LA (MeLELA) in male Wistar rats. Thirty rats (100-150 g) were equally distributed into 6 groups: Group I (vehicle-treated); group II received 2.5 mg/kg sodium arsenite (SA) thrice a week for 2 weeks; group III received streptozotocin (STZ, 50 mg/kg once); group IV received 200 mg/kg LA daily for 14 days; group V received SA and LA; group VI received STZ and LA. Sodium arsenite and STZ induced reno-hepatotoxicity and diabetes, respectively. Phytochemical screening, biomarkers/enzyme activities, blood glucose levels, micronucleus assay, kidney, liver and pancreas histologies were determined according to standard procedures. Alkaloids, carotenoids and flavonoids were present in abundance. Both SA-and STZ-treated groups recorded significant (p < 0.05) reductions in serum protein concentrations, while co-treatment with LA significantly restored the levels. The SA-induced significant increase in creatinine/urea levels were significantly reduced by LA. Co-treatment of each of SA-and STZ-treated groups, respectively, with LA significantly decreased the elevated serum alanine and aspartate aminotransferases' activities. Increased blood glucose level in diabetic group was remarkably lowered by LA. Also, the SA-induced frequency of micronucleated polychromatic erythrocytes was significantly ameliorated by LA. Conclusively, LA is protective against SA-induced toxicity and STZ-induced diabetes in Wistar rats.

Biochar Remediation Improves the Leaf Mineral Composition of Telfairia occidentalis Grown on Gas Flared Soil.

This study evaluates the effects of remediation of gas flared soil by biochar on the nutritional composition of cultivated Telfairia occidentalis leaves, relative to non-gas flared soil. Gas flared soils are degraded due to the presence of heavy metals, noxious gases, carbon soot and acidic rain. Biochar produced from oil palm fibre was applied at five different amounts: 0 t ha-1, 7.1 t ha-1, 13.9 t ha-1, 20.9 t ha-1 and 28.0 t ha-1 to containerized soils (both gas flared and control soil), inside a greenhouse, which were allowed to mineralize for two weeks. Two viable seeds of T. occidentalis per replicate were sown. After eight weeks of growth, leaves were harvested, dried and chemically analyzed. Application of biochar significantly increased leaf ash and crude fibre content of Telfairia occidentalis. Plants from soil treated with 13.9 t ha-1 of biochar had the highest concentrations of vitamins A, B1, B2, B6, C and E irrespective of soil type. Maximum increase in leaf vitamin and mineral content was obtained from leaves cultivated on gas flared soil treated with 13.9 t ha-1 and 7.1 t ha-1 of biochar respectively. The results show that biochar treatment can increase leaf mineral concentrations and that this effect is dependent on the amount of biochar application.

A comparative assessment of antiproliferative properties of resveratrol and ethanol leaf extract of Anogeissus leiocarpus (DC) Guill and Perr against HepG2 hepatocarcinoma cells.

BACKGROUND: Epidemiological and experimental evidences have shown cancer as a leading cause of death worldwide. Although the folklore use of plants as a reliable source of health-restoring principles is well-documented, the search for more of such plants that are active against diseases, such as cancer, continues. We report here a laboratory-based evidence of the relevance of an ethanol leaf extract of Anogeissus leiocarpus (A2L) in comparison with resveratrol, a natural polyphenol, in cancer therapy. METHODS: The quantitative assessment of flavonoid and phenolic contents involved quercetin and gallic acid as standards, respectively were determined using spectrophotometry. Cytotoxicity was determined fluorometrically using propidium-iodide-staining method. Antioxidant status, adenosine triphosphate (ATP) levels, caspase activities and mitochondrial integrity were assessed using fluorometry/luminometry. RESULTS: The antioxidant assay demonstrated that A2L possesses a strong antioxidant capacity as compared with the reference compounds, ascorbic acid and butylated hydroxytoluene. This is further buttressed by the significantly high level of phenolics obtained in the quantitative assessment of the extract. A 72-h post-treatment examination indicated that both A2L and resveratrol modulate the proliferation of HepG2 liver carcinoma cells in a time- and concentration-dependent manner. Determination of the total nuclei area, propidium-iodide negative and positive nuclei areas all further buttress the modulation of cell proliferation by A2L and resveratrol with the indication that the observed cell death is due to apoptosis and necrosis at lower and higher concentrations of treatments respectively. At lower concentrations (0.39-3.13 µg/mL), resveratrol possesses higher tendencies to activate caspases 3 and 7. Bioenergetically, both resveratrol and A2L do not adversely affect the cells at lower concentrations (0.39-6.25 µg/mL for resveratrol and 12.5-100.0 µg/mL for A2L) except at higher concentrations (12.5-25.0 µg/mL for resveratrol and 200-800 µg/mL for A2L) which are more pronounced in A2L-treated cells. Furthermore, the antioxidant status of HepG2 cells is not perturbed by resveratrol as compared with A2L. Assessment of 24-h post-treatment mitochondrial function shows that resveratrol is not mitotoxic as compared with A2L which exhibits mitotoxicity at its highest concentration. CONCLUSIONS: Taken together, findings from this study showed that A2L possesses strong antiproliferative activity and its prospect in the management of hepatocellular carcinoma deserves further investigation.

Methanol Extract of Adansonia digitata Leaf Protects Against Sodium Arsenite-induced Toxicities in Male Wistar Rats.

BACKGROUND: Human and animal population exposure to arsenic through the consumption of arsenic contaminated water is rampant in many parts of the world. Protective agents of medicinal plants origin could provide maximum protection against toxicities of various kinds. OBJECTIVE: The protective role of orally administered methanol extract of the leaves of Adansonia digitata (MELAD) on sodium arsenite (SA) - induced clastogenicity and hepatotoxicity in male Wistar rats was evaluated. MATERIALS AND METHODS: Thirty male Wistar rats divided into six Groups (1-6) of five animals each were used for the study. Group 1 (negative control) received distilled water and normal diet only, Groups 2-6 received the extract (at 250 or 500 mg/kg body weight) and/or SA at 2.5 mg/kg body weight. RESULTS: There was statistically significant (P < 0.05) increase in the number of micronucleated polychromatic erythrocytes and lipid peroxidation in the SA group as compared with the negative control and treated groups. Administration of the extract reduced the effects of SA on the above parameters. Activities of serum alanine and aspartate aminotransferases did not show statistically significant effects; however, the histological analyses revealed periportal cellular infiltration by mononuclear cells, whereas the MELAD treated groups show mild cellular infiltration and mild portal congestion. CONCLUSIONS: MELAD protect against SA-induced toxicities in rats, and it may offer protection in circumstances of co-exposure and cases of arsenicosis. SUMMARY: MELAD extract significantly reduce the lipid peroxidation induced by sodium arsenite in the liver of rats.MELAD did not show profound effects on the activities of serum alanine (ALT) and aspartate (AST) aminotranferases.MELAD offered significant protection against sodium arsenite-induced genotoxicity in the micronuclei induction assay.In the circumstances of co-exposure to arsenic contamination, MELAD may protect against sodium arsenite-induced toxicities. Abbreviations Used: MELAD: Methanol extract of the leaves of Adansonia digitata, SA: Sodium arsenite, nMPCEs: Number of micronucleated polychromatic erythocytes; ALT: Alanine aminotranferase; AST: Aspartate aminotranferase, TBARS: Thiobarbituric acid reactive substances, TBA: Thiobarbituric acid, MDA: malondialdehyde, Sodium arsenite (NaAsO2), IARC: International Agency for Research on Cancer.