Aims: Quercus infectoria (QI) gall extract is known to have broad spectrum anti-microbial activity in vitro. However, its mechanism of microbial growth inhibition is not well understood. The objectives of this study were to determine the antimicrobial effect of methanolic QI gall extract on bacteria and yeast and changes to their cell morphology. Methodology and results: The minimum inhibitory concentrations (MICs) of methanolic QI gall extract against Streptococcus agalactiae (ATCC 13813), Proteus vulgaris (ATCC 49312) and Candida albicans (ATCC 10231) were determined using two fold serial microdilution technique at concentrations ranging from 0.01 mg/mL to 5.00 mg/mL (for bacteria) and 0.02 mg/mL to 12.00 mg/mL (for yeast). Minimum bactericidal concentration (MBC) and minimum fungicidal concentration (MFC) were determined by subculturing the broth from the microtitre wells which showed no apparent growth or turbidity onto the nutrient agar plates. The scanning electron microscope (SEM) was used to analyze the morphology of bacteria and yeast cells treated with 1× MIC and 4× MIC of the extract. Substantial antimicrobial activity was observed against ATCC strains of S. agalactiae, P. vulgaris and C. albicans in this study. The MBC/MFC to MIC ratio (≤4) indicated the methanolic QI gall extract was bactericidal and fungicidal against all the tested strains. Changes to the cell morphology were more obvious at higher extract concentration (4× MIC). Conclusion, significance and impact of study: This study showed that QI gall extract has antimicrobial effects on the bacterial and yeast cell morphology and thus, provides scientific information suggesting its possible antimicrobial mechanisms on the cell wall and membrane integrity.

More studies are now focusing on vitamin E as an anticancer agent for its good effects in many in-vitro studies. Current studies proposed that vitamin E might be a suitable candidate as an alternative treatment for cancer due to its antioxidant properties. Vitamin E act as an antioxidant by their long-chain polyunsaturated fatty acids, and thus the integrity of membranes in the cells is maintained and consequently retain the bioactivity of the cells. This mini review will focus on the activity of vitamin E as an antioxidant to protect against cancer in in-vitro, in-vivo, and clinical studies. Although most studies reported great outcomes for the anticancer activity of vitamin E, there were some conflicting data. To date, studies on effects of vitamin E are still undergoing where researchers are still debating on the positive and negative effects of vitamin E as an anticancer therapeutic action.

Cancer-induced bone pain is currently facing inadequate pain management due to unwanted side effects and relative ineffectiveness. The search for alternative therapy to alleviate pain and target a few mechanism pathways might improve survival in metastatic patients. Vitamin E which has been promoted as anti-inflammatory, anti-cancer, and anti-metastatic were chosen in this study to potentiate its capability in a cancer-induced bone pain rat model. Rats were randomly grouped into five groups, and a breast cancer cell line was induced into the left femur of four groups: Negative Control (NC), Alpha Tocopherol (ATF), Tocotrienol Rich Fraction (TRF) and Zoledronic Acid (ZA), whereas Sham group as healthy subjects induced with supplementary media. Pain assessment tests were carried out at four days intervals. The animals were sacrificed after 21 days following SPECT/CT imaging. Bone specimens were analyzed for ELISA and gene expression studies. The results showed that the animal model was successfully validated via the presence of abnormal uptake of the skeletal system. Pain assessment tests demonstrated that vitamin E, specifically TRF significantly alleviate pain compared to the NC group. Biomarker activity illustrated that the TRF supplement group was able to regulate the bone turnover activity comparable to the ZA treatment group. Gene expression studies signify the role of TRF supplement comparable to the ZA group in the ability to regulate osteoclastogenesis, osteoclast activation, and regulating the secretion of metastatic cancer cytokine. This finding addressed the beneficial potency of TRF compared to ATF as a therapeutic option in the management of cancer-induced bone pain.