Forest vascular plants as indicators of plant species richness: A data analysis of a flora atlas from northwestern Germany

Abstract

Our study had the objective to examine whether the number of forest vascular plants in a forest-poor region may be indicative of total plant species richness and of the number of threatened plant species. We also related forest plant species richness to geological and soil variables. The analysis was based on a regional flora atlas from the Weser-Elbe region in northwestern Germany including incidence data of species in a total of 1109 grid cells (each ca. 2.8 × 2.8 km²). All taxa were classified either as forest or non-forest species. Total species richness in the grid cells ranged from 65 to 597, with a mean value of 308. The number of forest species varied between 20 and 309 (mean 176). Grid cells with or without particular geological units differed in total and forest species richness, with those containing peatland and marshland being particularly species-poor. Indicator value analysis showed that both total and forest species richness in the grid cells were related to soil acidity and nitrogen in a hump-backed manner, with the highest number of species found at moderately low values for nitrogen and at intermediate values of pH. Forest species richness was highly positively correlated with the number of non-forest species and threatened non-forest species. Indicators for high species richness were primarily those species that are confined to closed semi-natural forests with a varied topography and relatively base- and nutrient-rich soils. Grid cells including historically ancient forest exhibited a higher species richness than grid cells lacking ancient forest, indicating the importance of a long habitat continuity for a high phytodiversity. The “habitat coincidence” of high species richness is best explained by similar responses of forest species and species of other habitats to the main environmental gradients. It is suggested that the regional patterns found for the Weser-Elbe region can be transferred also to other forest-poor regions in Central Europe.     

Germination response of four pasture species to temperature,light, and post-harvest period

Abstract

The purpose of this research was to explore the effect of temperature, light, and post-harvest period, and their interactions, on seed germination ecology of four common pasture species in the Mediterranean environment. Mature seeds of Diplotaxis erucoides, Hirschfeldia incana, Hyoseris scabra (Mediterranean distribution) and Sonchus oleraceus (cosmopolitan distribution) were subjected to seven constant temperatures (10–40°C, at intervals of 5°C) under continuous darkness, or a 12 h/12 h light/dark photoperiod at 30, 150 and 270 days after harvest (DAH). Cumulative germination and germination speed were determined. In all the tested species, except S. oleraceus, light significantly enhanced germination. S. oleraceus seeds maintained germination values over 90%, in a wide range of temperatures (10–35°C), in the dark as well as in light. Seeds of H. incana germinated well soon after seed dispersal. In D. erucoides and H. scabra, germination increased with storage period, while in S. oleraceus there was no effect of seed age. In all the species, moreover, no germination was recorded at 40°C. Temperature, light, and post- harvest requirement may be regarded as an adaptation strategy to ensure optimal conditions for seedling development and survival in Mediterranean species, while the species with a cosmopolitan distribution germinates under almost all tested conditions.     

Ecogeographic and genetic evaluation of endemic species in the Maritime Alps: the case of Moehringia lebrunii and M. sedoides (Caryophyllaceae)

Abstract

The Maritime Alps are one of the ‘hot spots’ in the Mediterranean basin. This study investigated two endemic plants, Moehringia lebrunii and Moehringia sedoides (Caryophyllaceae) in order to increase knowledge of the vegetation of this region, and to investigate possible conservation strategies. Ecogeographic surveys and molecular analyses were undertaken. Gene diversity, the Shannon index and G_ST were calculated within and among populations of the two species based on ISSR data. The populations of M. lebrunii had a density ranging between 0.04 and 0.86 individual/m² and a rather low inner genetic variability value. According to IUCN Red List Criteria, the current status of M. lebrunii is Endangered [EN B2ab(ii, iv)]. M. sedoides is an endemic of the SW Alps (not exclusive of the Maritime Alps), and is very abundant within the core of the range. Its range of occurrence is smaller than previously reported; nevertheless, the species is not under threat. This taxon showed a population density ranging between 0.03 and 0.58 individual/m². Genetic variability values revealed a high variation among the species. Only peripheral populations seemed to suffer from their segregated position. Thus, M. sedoides is to be considered Critically Endangered [CR B1ab(i, ii, iii, iv) + 2ab(i, ii, iii, iv)] for Italy according to Regional Guidelines.     

Exercise training provides cardioprotection via a reduction in reactive oxygen species in rats submitted to myocardial infarction induced by isoproterenol

Exercise training has demonstrated cardioprotection effects. However, the exact mechanism behind this effect is not is clear. The present study evaluated the effects of 12 weeks of previous treadmill training on the levels of oxidative damage, antioxidant enzyme activity and injury in the myocardium of rats submitted to infarction induced by isoproterenol (ISO). Isoproterenol treatment (80 mg/kg given over 2 days in two equal doses) caused arrhythmias and 60% mortality within 24 h of the last injection in the control group (C + ISO) group when compared with the saline control group (saline). Creatine Kinase ? MB levels were markedly increased in hearts from ISO-treated animals in the C + ISO group. Twelve weeks of treadmill training reduced superoxide production, lipid peroxidation levels and protein carbonylation in these animals, as well as increasing the activities and expressions of SOD and CAT. Previous training also reduced CK-MB levels and numbers of deaths by 40%, preventing the deleterious effects of ISO. Based on the data obtained in this study, it is suggested that 12-week treadmill training increases antioxidant enzymes, decreases oxidative damage and reduces the degree of infarction induced by ISO in the hearts of male rats.     

Arguments against the significance of the Fenton reaction contributing to signal pathways under in vivo conditions

One of the common explanations for oxidative stress in the physiological milieu is based on the Fenton reaction, i.e. the assumption that radical chain reactions are initiated by metal-catalyzed electron transfer to hydrogen peroxide yielding hydroxyl radicals. On the other hand — especially in the context of so-called “iron switches” — it is postulated that cellular signaling pathways originate from the interaction of reduced iron with hydrogen peroxide.

Using fluorescence detection and EPR for identification of radical intermediates, we determined the rate of iron complexation by physiological buffer together with the reaction rate of concomitant hydroxylations of aromatic compounds under aerobic and anaerobic conditions. With the obtained overall reaction rate of 1,700 M^-1s^-1 for the buffer-dependent reactions and the known rates for Fenton reactions, we derive estimates for the relative reaction probabilities of both processes.

As a consequence we suggest that under in vivo conditions initiation of chain reactions by hydroxyl radicals generated by the Fenton reaction is of minor importance and hence metal-dependent oxidative stress must be rather independent of the so-called “peroxide tone”. Furthermore, it is proposed that — in the low (subtoxic) concentration range — hydroxylated compounds derived from reactions of “non-free” (crypto) OH radicals are better candidates for iron-dependent sensing of redox-states and for explaining the origin of cellular signals than the generation of “free” hydroxyl radicals.     

Mitochondrial reactive oxygen species originating from Romo1 exert an important role in normal cell cycle progression by regulating p27Kip1 expression

Reactive oxygen species (ROS) steady-state levels are required for entry into the S phase of the cell cycle in normal cells, as well as in tumour cells. However, the contribution of mitochondrial ROS to normal cell proliferation has not been well investigated thus far. A previous report showed that Romo1 was responsible for the high ROS levels in tumour cells. Here, we show that endogenous ROS generated by Romo1 are indispensable for cell cycle transition from G1 to S phase in normal WI-38 human lung fibroblasts. The ROS level in these cells was down-regulated by Romo1 knockdown, resulting in cell cycle arrest in the G1 phase. This arrest was associated with an increase in the level of p27^Kip1. These results demonstrate that mitochondrial ROS generated by Romo1 expression is required for normal cell proliferation and it is suggested that Romo1 plays an important role in redox signalling during normal cell proliferation.     

Retinol supplementation induces oxidative stress and modulates antioxidant enzyme activities in rat Sertoli cells

Recent intervention studies revealed that supplementation with retinoids resulted in a higher incidence of lung cancer. Recently the causal mechanism has begun to be clarified. We report here that retinol caused cellular oxidative stress and modulated superoxide dismutase, catalase and glutathione peroxidase activities. Retinol (7 μM) significantly increased TBARS, conjugated dienes, and hydroperoxide-initiated chemiluminescence in cultured Sertoli cells. In response to retinol treatment superoxide dismutase, catalase and glutathione peroxidase activities increased. TBARS content and catalase activities were decreased by a free radical scavenger. These findings suggest that retinol may induce oxidative stress and modulate antioxidant enzyme activities in Sertoli cells.     

Reactive oxygen species in cancer

Abstract

Elevated rates of reactive oxygen species (ROS) have been detected in almost all cancers, where they promote many aspects of tumour development and progression. However, tumour cells also express increased levels of antioxidant proteins to detoxify from ROS, suggesting that a delicate balance of intracellular ROS levels is required for cancer cell function. Further, the radical generated, the location of its generation, as well as the local concentration is important for the cellular functions of ROS in cancer. A challenge for novel therapeutic strategies will be the fine tuning of intracellular ROS signalling to effectively deprive cells from ROS-induced tumour promoting events, towards tipping the balance to ROS-induced apoptotic signalling. Alternatively, therapeutic antioxidants may prevent early events in tumour development, where ROS are important. However, to effectively target cancer cells specific ROS-sensing signalling pathways that mediate the diverse stress-regulated cellular functions need to be identified. This review discusses the generation of ROS within tumour cells, their detoxification, their cellular effects, as well as the major signalling cascades they utilize, but also provides an outlook on their modulation in therapeutics.     

Oxidative stress and aging in Caenorhabditis elegans

Much attention has been focused on the hypothesis that oxidative damage plays in cellular and organismal aging. A mev-1 (kn1) mutant of Caenorhabditis elegans, isolated on the basis of its methyl viologen (paraquat) hypersensitivity, is also hypersensitive to elevated oxygen levels. Unlike the wild type, its life span decreases dramatically as oxygen concentrations are increased from 1% to 60%. Strains, which bear this mutation, accumulate fluorescent materials and protein carbonyl groups, markers of aging, at faster rates than the wild type. We have cloned mev-1 gene by transformation rescue and found that it is, in fact, the previously sequenced gene (cyt-1) that encodes succinate dehydrogenase cytochrome b. A missense mutation abolishes complex II activity in the mitochondrial membrane but not succinate dehydrogenase enzyme activity per se. These data suggest that CYT-1 directly participates in electron transport from FADH₂ to coenzyme Q. Moreover, mutational inactivation of this process renders animals susceptible to oxidative stress and, as a result, leads to premature aging.     

Global overexpression of divalent metal transporter 1 delays crocidolite-induced mesothelial carcinogenesis in male mice

Abstract

Exposure to asbestos fiber is central to mesothelial carcinogenesis, for which iron overload in or near mesothelial cells is a key pathogenic mechanism. Alternatively, iron chelation therapy with deferasirox or regular phlebotomy was significantly preventive against crocidolite-induced mesothelial carcinogenesis in rats. However, the role of iron transporters during asbestos-induced carcinogenesis remains elusive. Here, we studied the role of divalent metal transporter 1 (DMT1; Slc11a2), which is a Fe(II) transporter, that is present not only on the apical plasma membrane of duodenal cells but also on the lysosomal membrane of every cell, in crocidolite-induced mesothelial carcinogenesis using DMT1 transgenic (DMT1Tg) mice. DMT1Tg mice show mucosal block of iron absorption without cancer susceptibility under normal diet. We unexpectedly found that superoxide production was significantly decreased upon stimulation with crocidolite both in neutrophils and macrophages of DMT1Tg mice, and the macrophage surface revealed higher iron content 1?h after contact with crocidolite. Intraperitoneal injection of 3?mg crocidolite ultimately induced malignant mesothelioma in ～50% of both wild-type and DMT1Tg mice (23/47 and 14/28, respectively); this effect was marginally (p?=?0.069) delayed in DMT1Tg mice, promoting survival. The promotional effect of nitrilotriacetic acid was limited, and the liver showed significantly higher iron content both in DMT1Tg mice and after crocidolite exposure. The results indicate that global DMT1 overexpression causes decreased superoxide generation upon stimulation in inflammatory cells, which presumably delayed the promotional stage of crocidolite-induced mesothelial carcinogenesis. DMT1Tg mice with low-stamina inflammatory cells may be helpful to evaluate the involvement of inflammation in various pathologies.