Impact of zinc,selenium and lycopene on capsaicin induced mutagenicity and oxidative damage in mice

Capsaicin is employed as a condiment and colorant in the cosmetic and pharmaceutical industries. Metabolism of capsaicin produces reactive phenoxy radicals, which inflict damage to DNA. Micronutrients such as zinc and selenium facilitate the expression of tissue repair factors, and lycopene has natural antioxidant action. The current study investigated the possible protective role of zinc, selenium and lycopene singly and in combination in ameliorating capsaicin induced mutagenicity. Fifty four Swiss albino mice received the vehicle, zinc (10 mg/kg), selenium (2 mg/kg), lycopene (2 mg/kg) alone, capsaicin alone (2 mg/kg), and capsaicin along with zinc (10 mg/kg), selenium (2 mg/kg) and lycopene (2 mg/kg) in combination by the oral route for 32 days. Animals were killed 24 h after the last treatment, and micronuclei formation in bone marrow and peripheral blood were assessed. Antioxidant status in plasma, the total protein, nucleic acids, and DNA fragmentation was assessed in the liver homogenate. Capsaicin substantially damaged nuclear material and increased oxidative stress. Individual therapy with lycopene was most effective in reducing micronuclei formation, lipid peroxidation, and in augmenting ferric reducing ability of plasma. This was closely followed by zinc and selenium. Zinc protected against DNA fragmentation followed by lycopene and selenium. The combination therapy was effective over individual treatment against DNA fragmentation, micronuclei and malondialdehyde formation. The combination did not exert a substantial benefit over individual therapy in enhancing the total antioxidant ability of plasma. The risk of capsaicin induced mutagenicity was lowered with the combination by reducing the generation of free radicals and by enhancing tissue repair.     

Nitrogen deposition drives lichen community changes through differential species responses

Nitrogen (N) deposition has increased globally over the last 150 years and further increases are predicted. Epiphytic lichens decline in abundance and diversity in areas with high N loads, and the abundance of lichens decreases along gradients of increased deposition. Thus, although N is an essential nutrient for lichens, excessive loads may be detrimental for them. However, these gradients include many correlated pollutants and the mechanisms behind the decline are thus poorly known. The aim of this study was to assess effects of N deposition, alone, on the epiphytic lichen community composition in a naturally N‐poor boreal forest. For this purpose, whole spruce trees were fertilized daily with N at five levels, equivalent to 0.6, 6, 12.5, 25, and 50 kg N ha^?1 yr^?1, during four consecutive growing seasons (2006–2009), and changes in the abundance of lichens were monitored each autumn from the preceding year (2005). The studied lichen communities were highly dynamic and responded strongly to the environmental perturbation. N deposition detectably altered the direction of succession and reduced the species richness of the epiphytic lichen communities, even at the lowest fertilization application (6 kg N ha^?1 yr^?1). The simulated N deposition caused significant changes in the abundance of Alectoria sarmentosa, Bryoria spp., and Hypogymnia physodes, which all increased at low N loads and decreased at high loads, but with species‐specific optima. The rapid decline of A. sarmentosa may have been caused by the added nitrogen reducing the stability of the lichen thalli, possibly due to increases in the photobiont: mycobiont ratio or parasitic fungal attacks. We conclude that increases in nitrogen availability, per se, could be responsible for the reductions in lichen abundance and diversity observed along deposition gradients, and those community responses may be due to physiological responses of the individual species rather than changes in competitive interactions.