Temperature stress and survival ability of Mediterranean sclerophyllous plants

ABSTRACT

The Mediterranean climate with hot and dry summer periods, and low winter temperatures and episodic frosts in northern, altitudinal and continental districts, demands from evergreen broadleaved woody plants an adequate and flexible acclimation to the climatic constraints.

In this brief survey on some responses of Mediterranean sclerophylls to temperature stress, the following is presented and discussed: criteria for cold and heat limits of photosynthetic function; winter depression and summer photoinactivation of photosynthesis; peculiar patterns of tissue freezing of scleromorphous leaves and limits of frost resistance of various plant parts and ontogenetic stages; heat impairment of chloroplasts and thermotolerance of sclerophyllous species; survival capacity and recovery after damage. Risks of damage to plants in relation to stressful temperatures in Mediterranean regions are estimated. Cold stress and drought stress indices, according to Mitrakos (1980), have been applied to characterise different localities in Italy. Additionally, a heat stress index for the Mediterranean region is proposed. Future research topics are suggested.     

Specific root length as an indicator of environmental change

Abstract

Specific root length (SRL, m g^?1) is probably the most frequently measured morphological parameter of fine roots. It is believed to characterize economic aspects of the root system and to be indicative of environmental changes. The main objectives of this paper were to review and summarize the published SRL data for different tree species throughout Europe and to assess SRL under varying environmental conditions. Meta-analysis was used to summarize the response of SRL to the following manipulated environmental conditions: fertilization, irrigation, elevated temperature, elevated CO₂, Al-stress, reduced light, heavy metal stress and physical disturbance of soil. SRL was found to be strongly dependent on the fine root classes, i.e. on the ectomycorrhizal short roots (ECM), and on the roots <0.5 mm, <1 mm, <2 mm and 1 – 2 mm in diameter SRL was largest for ECM and decreased with increasing diameter. Changes in soil factors influenced most strongly the SRL of ECM and roots <0.5 mm. The variation in the SRL components, root diameter and root tissue density, and their impact on the SRL value were computed. Meta-analyses showed that SRL decreased significantly under fertilization and Al-stress; it responded negatively to reduced light, elevated temperature and CO_2. We suggest that SRL can be used successfully as an indicator of nutrient availability to trees in experimental conditions.     

Effect of spatial and temporal patterns of stress and disturbance intensities in a sub-Mediterranean grassland

Abstract

The present study examined a sub-Mediterranean pastoral system in the central Apennines (Italy) with a long history of grazing, where winter cold stress is alternated with summer drought stress. The research goals were to ascertain whether different floristic structures correspond to different stress conditions (xeric and semimesic), and whether peculiar functional plant traits (such as avoidance and tolerance mechanisms) respond to stress/disturbance intensities, and understand how vegetation reacts to changeable livestock pressure (through floristic and plant trait variations). Cluster analysis indicated that separate communities develop under different stress intensities. Other analyses highlighted how avoidance strategies predominate within the pastoral system. Observations of grazed and ungrazed patches conducted in 10-m transects revealed spiny cushion formation in semimesic grassland, where a brief period of overgrazing occurs in late summer, causing variations in plant community structure. All these results confirm the importance of historical grazing and current land use, showing how small disturbances and stress variations cause ecosystem responses. Best practices for management were identified. In xeric conditions, it is advisable that the intensity of disturbance be lessened, while in semimesic grassland overgrazing should be forbidden during the dry period, because it could facilitate the development of spiny patches, and subsequent spread of Brachypodium rupestre.     

Anticarcinogenic antioxidants as inhibitors against intracellular oxidative stress

Oxidative stress has been implicated in the pathogenesis of numerous diseases, including cancer. In the present study, the protective effect of natural antioxidants, such as quercetin and tea polyphenols, on intracellular oxidative stress was studied. Here we report a novel function of quercetin and tea polyphenols, as potential inhibitors of 4-hydroxy-2-nonenal (HNE)-induced intracellular oxidative stress and cytotoxicity. In rat liver epithelial RL34 cells, a potent electrophile HNE dramatically induced the productions of reactive oxygen species (ROS), which correlated well with the reduction in cell viability. We found that quercetin and tea polyphenols, such as epigallocatechin gallate and theaflavins and their gallate esters, significantly inhibited the HNE-induced ROS production and cytotoxicity. In addition, HNE induced a transient decrease in the mitochondrial membrane potential (Δψ), which was also retarded by the antioxidants. These data suggest that the antioxidants, such as quercetin and tea polyphenols, are inhibitors against mitochondrial ROS production.     

Vinpocetine attenuates the metabolic dysfunction induced by amyloid β-peptides in PC12 cells

The cytoprotective effect of vinpocetine [14-ethoxycarbonyl-(3α,16α-ethyl)-14,15-eburnamine] was investigated on PC12 cells treated with the amyloid β-peptides (Aβ) for 24 hours. Vinpocetine was shown to protect cells from the inhibition in redox status induced by exposure to Aβ_25–35 and Aβ_1–40, the maximal protection being achieved at a vinpocetine concentration of 40 μM. At this concentration, vinpocetine blocked the inhibition of the mitochondrial respiratory chain complexes II–III and IV and completely abolished the depletion of pyruvate levels induced by toxic concentrations of Aβ peptides. Furthermore, the accumulation of ROS in cells exposed to Aβ_25–35 and Aβ_1–40 evaluated using the fluorescent probe 2′,7′-dichlorofluorescin (DCF), was reduced in the presence of 40 μM vinpocetine. Taken together, the data presented herein demonstrate that vinpocetine protects cells from Aβ toxicity, preventing the generation of oxidative stress due to the excessive accumulation of ROS. This study suggests that vinpocetine can exert neuroprotective properties which might be of importance and contribute to its clinical efficacy in the treatment of Alzheimer's disease or other neurodegenerative disorders in which oxidative stress is involved.     

Lipid and protein oxidation in hepatic homogenates and cell membranes exposed to bile acids

Cholestasis occurs in a variety of hepatic diseases and causes damage due to accumulation of bile acids in the liver. The aim was to investigate the effect of several bile acids, i.e. chenodeoxycholic, taurochenodeoxycholic, deoxycholic, taurodeoxycholic, ursodeoxycholic, lithocholic and taurolithocholic (TLC), in inducing oxidative damage. Hepatic tissue of male Sprague-Dawley rats was incubated with or without 1 mM of each bile acid, with or without 0.1 mM FeCl₃ and 0.1 mM ascorbic acid for the purpose of generating free radicals. Several bile acids increased lipid and protein oxidation, with TLC being the most pro-oxidative (657% and 175% in homogenates and 350% and 311% in membranes, respectively). TLC also enhanced iron-induced oxidative stress to lipids (21% in homogenates and 29% in membranes) and to proteins (74% in membranes). This enhancement was dose- and time-dependent and was reduced by melatonin. These results suggest that bile acids differentially mediate hepatic oxidative stress and may be involved in the physiopathology of cholestasis.     

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.     

Patterns of RNA and Protein Synthesis in Post-Ischemic Livers

The re-establishment of the blood supply to a formerly ischemic liver lobe, before the “point of no return” of the tissue is reached, induces a series of changes in protein and RNA metabolism that are functional to the repair of the damage suffered by the cells. Among these events there is the increase, in synthesis of a group of proteins known as heat-shock (or stress) proteins, which are also induced in liver cells by different kinds of oxidative stress. The increase in synthesis of these proteins is largely due to the activation of their genes: some of these genes are also activated in cells stimulated to grow.

These observations suggest a link between oxidative stress, repair of cell damage and cell multiplication.