Vernonia calvoana Shows Promise towards the Treatment of Ovarian Cancer.

The treatment for ovarian cancers includes chemotherapies which use drugs such as cisplatin, paclitaxel, carboplatin, platinum, taxanes, or their combination, and other molecular target therapies. However, these current therapies are often accompanied with side effects. Vernonia calvoana (VC) is a valuable edible medicinal plant that is widespread in West Africa. In vitro data in our lab demonstrated that VC crude extract inhibits human ovarian cancer cells in a dose-dependent manner, suggesting its antitumor activity. From the VC crude extract, we have generated 10 fractions and VC fraction 7 (F7) appears to show the highest antitumor activity towards ovarian cancer cells. However, the mechanisms by which VC F7 exerts its antitumor activity in cancer cells remain largely unknown. We hypothesized that VC F7 inhibits cell proliferation and induces DNA damage and cell cycle arrest in ovarian cells through oxidative stress. To test our hypothesis, we extracted and fractionated VC leaves. The effects of VC F7 were tested in OVCAR-3 cells. Viability was assessed by the means of MTS assay. Cell morphology was analyzed by acridine orange and propidium iodide (AO/PI) dye using a fluorescent microscope. Oxidative stress biomarkers were evaluated by the means of lipid peroxidation, catalase, and glutathione peroxidase assays, respectively. The degree of DNA damage was assessed by comet assay. Cell cycle distribution was assessed by flow cytometry. Data generated from the MTS assay demonstrated that VC F7 inhibits the growth of OVCAR-3 cells in a dose-dependent manner, showing a gradual increase in the loss of viability in VC F7-treated cells. Data obtained from the AO/PI dye assessment revealed morphological alterations and exhibited characteristics such as loss of cellular membrane integrity, cell shrinkage, cell membrane damage, organelle breakdown, and detachment from the culture plate. We observed a significant increase (p < 0.05) in the levels of malondialdhyde (MDA) production in treated cells compared to the control. A gradual decrease in both catalase and glutathione peroxidase activities were observed in the treated cells compared to the control. Data obtained from the comet assay showed a significant increase (p < 0.05) in the percentages of DNA cleavage and comet tail length. The results of the flow cytometry analysis indicated VC F7 treatment caused cell cycle arrest at the S-phase checkpoint. Taken together, our results demonstrate that VC F7 exerts its anticancer activity by inhibiting cell proliferation, inducing DNA damage, and causing cell cycle arrest through oxidative stress in OVAR-3 cells. This finding suggests that VC F7 may be a potential alternative dietary agent for the prevention and/or treatment of ovarian cancer.

Prostate Cancer Disparity, Chemoprevention, and Treatment by Specific Medicinal Plants.

Prostate cancer (PC) is one of the most common cancers in men. The global burden of this disease is rising. Its incidence and mortality rates are higher in African American (AA) men compared to white men and other ethnic groups. The treatment decisions for PC are based exclusively on histological architecture, prostate-specific antigen (PSA) levels, and local disease state. Despite advances in screening for and early detection of PC, a large percentage of men continue to be diagnosed with metastatic disease including about 20% of men affected with a high mortality rate within the African American population. As such, this population group may benefit from edible natural products that are safe with a low cost. Hence, the central goal of this article is to highlight PC disparity associated with nutritional factors and highlight chemo-preventive agents from medicinal plants that are more likely to reduce PC. To reach this central goal, we searched the PubMed Central database and the Google Scholar website for relevant papers. Our search results revealed that there are significant improvements in PC statistics among white men and other ethnic groups. However, its mortality rate remains significantly high among AA men. In addition, there are limited studies that have addressed the benefits of medicinal plants as chemo-preventive agents for PC treatment, especially among AA men. This review paper addresses this knowledge gap by discussing PC disparity associated with nutritional factors and highlighting the biomedical significance of three medicinal plants (curcumin, garlic, and Vernonia amygdalina) that show a great potential to prevent/treat PC, as well as to reduce its incidence/prevalence and mortality, improve survival rate, and reduce PC-related health disparity.

ß-ESTRADIOL INDUCES CYTOTOXIC EFFECTS TO HUMAN T-LYMPHOMA (JURKAT) CELLS THROUGH OXIDATIVE STRESS.

ß-estradiol is the most potent estrogen of a group of endogenous estrogen steroids which includes estrone and estriol. This steroid hormone is the most potent natural estrogen, produced mainly by the ovary, placenta, and in smaller amounts by the adrenal cortex, and the male testes. Although ß-estradiol protects the renal and cardiovascular systems, the mechanisms involved remain unclear. In this research, we performed the MTT [3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay to evaluate the effect of ß-estradiol on human T-lymphoma (Jurkat) cells upon 24 and 48 hours, respectively. Lipid peroxidation assay was also performed to estimate the levels of malondialdehyde (MDA) production in ß-estradiol-treated cells. The results of MTT assay demonstrated that low, physiological levels of ß-estradiol induce cellular proliferation in Jurkat T-cells. At higher dose of exposure, ß-estradiol decreases the viability of Jurkat T-cells compared to the control cells. Data generated from lipid peroxidation assay resulted in a significant increase (p < 0.05) in MDA production in ß-estradiol treated sample. Upon 48 h of exposure, MDA concentrations in the sample [µM] (mean ±SE, n = 3) compared to untreated control were 4.9 ± 1.7, 8.1 ± 1,6 11.5 ± 2.2, 21.1 ± 2.3, 19.5 ± 1.4, and 21.5 ± 2.6 in 0, 1, 2, 4, 8, and 16 µM ß-estradiol, respectively. In summary, findings from this study demonstrated that high dose of ß-estradiol is cytotoxic to Jurkat T-cells. This cytotoxicity is found to be associated with oxidative stress.