Improving Whole Tomato Transformation for Prostate Health: Benign Prostate Hypertrophy as an Exploratory Model.

It is well-established that the beneficial properties of single phytonutrients can be better attained when they are taken with the complex of the molecules present in their natural milieu. Tomato, the fruit providing the most comprehensive complex of prostate-health-preserving micronutrients, has been shown to be superior to its single-nutrient counterparts in decreasing the incidence of age-related prostate diseases. Herein, we describe a novel tomato food supplement enriched with olive polyphenols, containing cis-lycopene concentrations far exceeding those present in industry-produced tomato commodities. The supplement, endowed with antioxidant activity comparable to that of N-acetylcysteine, significantly reduced, in experimental animals, the blood levels of prostate-cancer-promoting cytokines. In prospective, randomized, double-blinded, placebo-controlled studies performed on patients affected by benign prostatic hyperplasia, its uptake significantly improved urinary symptoms and quality of life. Therefore, this supplement can complement and, in some cases, be an alternative to current benign prostatic hyperplasia management. Furthermore, the product suppressed carcinogenesis in the TRAMP mouse model of human prostate cancer and interfered with prostate cancer molecular signaling. Thus, it may offer a step forward in exploring the potential of tomato consumption to delay or prevent the onset of age-related prostate diseases in high-risk individuals.

Development of the whole tomato and olive-based food supplement enriched with anti-platelet aggregating nutrients.

BACKGROUND: Platelet dysfunctions are shared by cardiovascular diseases and a wide range of inflammatory diseases. AIMS: To determine the ability of a new whole tomato-based food supplement (WTBFS) containing carotenoid and olive polyphenols to inhibit platelet aggregation. METHODS: Aggregation was evaluated in platelet-rich plasma using microtiter plates and a plate reader. RESULTS: Platelets treated with WTBFS showed a >70% reduction of 5 µM adenosine diphosphate (ADP)-induced platelet aggregation; at 10 µM of ADP, the inhibitory effect of WTBFS was reduced of about 50%. Similarly, 78% and 48% reduction were obtained using 5 µg/mL and 10 µg /mL of collagen as an agonist. CONCLUSION: Since the compounds in WTBFS share the ability to inhibit STAT3, the inhibition of its signaling pathway may represent the mechanism underlying the antiplatelet activities. The activity of a lipophilic solution prepared from WTBS was in vitro tested on the platelet aggregation in response to ADP agonists and Collagen.

Serum levels of tumor necrosis factor-alpha in patients with psoriasis before, during and after narrow-band UVB phototherapy.

BACKGROUND: Narrow-band UVB (NB-UVB) phototherapy is widely used worldwide for moderate and severe psoriasis, which is a chronic autoimmune inflammatory disease characterized by skin infiltrates of Th1-, Th17- and Th22-cells releasing locally pro-inflammatory cytokines. We investigate serum levels of tumor necrosis factor-α (TNF-α) in psoriatic patients before and after NB-UVB phototherapy. METHODS: Twenty-eight subjects with moderate/severe plaque type psoriasis were enrolled. The severity of skin involvement was rated according to the Psoriasis Area and Severity Index (PASI) score at baseline (T0) and after 4 (T1) and 12 (T2) weeks of NB-UVB treatment. At the same time points, blood samples were taken for evaluation of TNF-α levels. NB-UVB phototherapy was administered twice weekly on non-consecutive days until 12 weeks. RESULTS: The median PASI score significantly decreased from 12.0 at baseline (T0), to 6.9 after 4 weeks (T1, P<0.001) and to 0 after 12 weeks (T2, P<0.001). TNF-a serum levels significantly increased in respect to the baseline after 12 weeks of therapy. CONCLUSIONS: NB-UVB phototherapy is highly effective against psoriasis but, as it increases the TNF-α serum level, it seems unlikely that it can decrease the chronic inflammatory state that is thought to be responsible of the systemic co-morbidities of psoriasis.