Gamma rays induced acquisition of structural modification in chitosan boosts photosynthetic machinery, enzymatic activities and essential oil production in citronella grass (Cymbopogon winterianus Jowitt).

Oligomers derived through irradiation of marine polysaccharides have generated a lot of interest of plant biologists as the application of these molecules has yielded positive results regarding various plant processes. To comprehend the previously established growth-promoting activity of irradiated chitosan (ICH) and to gain insight of the structure-property relationship, gamma rays induced structural changes were analyzed using techniques such as Fourier Transform Infrared (FT-IR) spectroscopy, Ultraviolet-visible (UV-Vis) spectroscopy, 13C-Nuclear Magnetic Resonance (NMR) spectroscopy and Scanning Electron Microscopy (SEM). Moreover, to study the bioactivity of ICH samples a pot experiment was conducted on citronella grass (Cymbopogon winterianus) to access its response to foliar application of various levels (40, 60, 80 and 100 mg L-1) of ICH in terms of growth, physiological attributes and essential oil (EO) production. The application of ICH at 80 mg L-1(ICH-80) resulted in the maximum values of most of the attributes studied. Due to this treatment, the maximum improvement in the content (29.58%) and yield (90.81%) of EO in Cymbopogon winterianus were achieved. Gas chromatography-mass spectrometry (GC-MS) analysis revealed that ICH-80 also increased the content of citronellal (14.81%) and geraniol (18.15%) of the EO as compared to the control.

Combination Effect of δ-Tocotrienol and γ-Tocopherol on Prostate Cancer Cell Growth.

Tocotrienols (T3s) and tocopherols (Tocs) are both members of the vitamin E family. It is known that δ-tocotrienol (δ-T3) has displayed the most potent anti-cancer activity amongst the tocotrienols. On the other hand, γ-tocopherol (γ-Toc) is reported to have a protective effect against prostate cancer. Therefore, we investigated whether the combination of γ-Toc and δ-T3 could strengthen the inhibitory effect of δ-T3 on prostate cancer cell growth. In this study the effect of combined δ-T3 (annatto T3 oil) and γ-Toc (Tmix, γ-Toc-rich oil) therapy was assessed against human androgen-dependent prostate cancer cells (LNCaP). We found that combined treatment of δ-T3 (10 µM) and γ-Toc (5 µM) resulted in reinforced anti-prostate cancer activity. Specifically, cell cycle phase distribution analysis revealed that in addition to G1 arrest caused by the treatment with δ-T3, the combination of δ-T3 with γ-Toc induced G2/M arrest. Enhanced induction of apoptosis by the combined treatment was also observed. These findings indicate that combination of δ-T3 and γ-Toc significantly inhibits prostate cancer cell growth due to the simultaneous cell cycle arrest in the G1 phase and G2/M phase.

Lycopene and the LXRα agonist T0901317 synergistically inhibit the proliferation of androgen-independent prostate cancer cells via the PPARγ-LXRα-ABCA1 pathway.

In our previous study, we demonstrated that lycopene can inhibit the proliferation of androgen-dependent prostate LNCaP cancer cells through the activation of the peroxisome proliferator-activated receptor gamma (PPARγ)-liver X receptor alpha (LXRα)-ATP-binding cassette transporter 1 (ABCA1) pathway. However, it is still unclear whether lycopene possesses similar effects in androgen-independent prostate cancer cells DU145 and PC-3. As lycopene inhibited the proliferation of both cell types to a similar extent, we chose DU145 cells for most of the subsequent studies. We show that lycopene significantly increased protein and mRNA expression of PPARγ, LXRα and ABCA1 and cholesterol efflux (i.e., decreased cellular cholesterol and increased cholesterol in culture medium). Lycopene (10 µM) in the presence of a specific antagonist of PPARγ (GW9662) or of LXRα (GGPP) restored the proliferation of DU145 cells and significantly suppressed lycopene-induced protein and mRNA expression of PPARγ and LXRα and cholesterol efflux. Liver X receptor α knockdown by siRNA against LXRα significantly promoted the proliferation of DU145 cells, whereas si-LXRα knockdown followed by incubation with lycopene (10 µM) restored the proliferation to the control level. Furthermore, lycopene in combination with the LXRα agonist T0901317 exhibited synergistic effects on cell proliferation and protein expression of PPARγ, LXRα and ABCA1. These results demonstrate that lycopene can inhibit DU145 cell proliferation via PPARγ-LXRα-ABCA1 pathway and that lycopene and T0901317 exhibit synergistic effects.