Photodynamic antimicrobial chemotherapy is a pathway for consideration of cell death of many microorganisms in biology such as bacteria. Various photo-sensitizer compounds were used in this technique such as porphyrin compounds. In this work, the effect of various concentrations of cationic porphyrin compounds was investigated and compared on cell death of S. aureus and E. coli by means of a 100 watt tungsten lamp.

Prostate cancer is the second leading cause of cancer-related deaths in America. An estimated 220,800 new cases and 27,540 cancer-related deaths are expected in the year 2015. Reactive Oxygen Species (ROS) can promote cancer cell proliferation when they reach elevated levels. Vitamin C (Vit C) is a water-soluble antioxidant capable of inhibiting the formation of ROS. Genistein(Gn), an isoflavone found in plants, also possesses the ability to inhibit ROS formation. The purpose of this study was to investigate the impact of vitamin C on genistein-induced apoptosis in LNCaP cells and the potential pathways involve, using cell-based assays including: MTT assay to determine the effect of the various treatments (Gn, Vit C and Gn+Vit C combination) on LNCaP; Nitroblue tetrazolium assay (NBT) to assess treatment-induced intracellular ROS levels; Fluorescence microscopy to determine the mode of treatment-induced cell death.  Briefly, LNCaP cells were exposed to varying concentrations of genistein (Gn_{10-70 uM} ) and vitamin C (C_10-70uM) as single treatments, and Gn-VitC combination. For Gn-VitC combination regiment, the IC50 (40uM) of the Vit C (previously determined), was used with each concentration of the genistein. Post-treatment effects on the cells were assessed after 48 hr, using the assays listed above.

The overall data from the result revealed a dose-dependent effect in all the three treatments, and apoptosis as the major mode of cell death and that vitamin C significantly augmented the effects of genistein. The combination treatment showed the most dramatic effect, causing most apoptosis. Details of the overall data implicates ROS in the treatment-induced apoptosis and significant positive impact of vitamin C on genistein treatment: an indication of the potential chemo/phyto-preventive significance of the nutrients. Further studies are in progress.

Plethora of studies has reiterated the importance of chemoprevention in the reduction of prostate cancer (PCa) incidence and death rate in recent years. However an estimated 220,800 new prostate cancer cases and 27,540 deaths are expected to occur in US men by the end of 2015. Beta-lapachone is a promising anticancer bioreductive ortho-naphthoquinone that was initially isolated from the bark of the South American Lapacho tree. Recent studies suggest that β-lap kills cancer cells targeting the NAD(P)H:quinone oxidoreductase (NQO1) enzyme levels in cancer tissues. But LNCaP, a cell line of primary and metastatic hormone dependent PCa is deficient in NQO1 enzyme. In this study, the potential role of very low doses of x-ray radiation (VLDR) from a portable pyroelectric generator at 20mGy/hr in enhancing the chemopreventive effects of beta-lapachone in LNCaP cells were investigated. This generator uses the pyroelectric principle to generate low doses of low energy radiation from polarized pyroelectric crystal when heated or cooled. Chemosensitivity by exposing LNCaP (and/or PC3) cells to 20mGy/hr of x-ray radiation prior to treatment with varied dose concentrations of beta-lapachone, we assessed the using MTT and Trypan blue exclusion assays. Dicoumarol (an NQO1 inhibitor) was administered to assess the effect of VLDR on NQO1 activation. Nitroblue tetrazolium assay was used to assess the intracellular ROS levels. Fluorescence microscopy and DNA Fragmentation were used to assess the mode of cell death. LNCaP cells were found to be slightly more radiosensitive compared to PC3 cells after exposure to VLDR. The data suggests that VLDR induced a rise in ROS levels, followed by upregulation in NQO1 levels. The major mode of cell death by this combination therapy was found to be via Apoptosis. In conclusion, our results confirm that VLDR-induced NQO1 levels contribute to LNCaP cell death by enhancing the chemopreventive effects of beta-lapachone.