ISSN: 2325-9655

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Editorial, Expert Opin Environ Biol Vol: 1 Issue: 1

Environmental Stress on Animals: Adverse or Beneficial?

Christian E.W. Steinberg*
Department of Biology, Humboldt-Universität zu Berlin, Berlin
Corresponding author : Christian E.W. Steinberg
Humboldt-Universität zu Berlin, Department of Biology, Laboratory of Freshwater and Stress Ecology, Späthstr, 80/81, 12437 Berlin
Received: September 18, 2012 Accepted: September 19, 2012 Published: September 21, 2012
Citation: Steinberg CEW (2012) Environmental Stress on Animals: Adverse or Beneficial? Expert Opin Environ Biol 1:1. doi:10.4172/2325-9655.1000e104


Environmental Stress on Animals: Adverse or Beneficial?

“Stress” – this word has an ugly sound in the public opinion, and usually, stress is considered adverse: too much work load, or, conversely, unemployment; lack of success; unsolved family problems, etc. Such personal experience may have blinded many scholars to study environmental stresses and their impact on organisms, particularly on animals, more relaxed, more scientifically based and without personal bias.

“Stress” – this word has an ugly sound in the public opinion, and usually, stress is considered adverse: too much work load, or, conversely, unemployment; lack of success; unsolved family problems, etc. Such personal experience may have blinded many scholars to study environmental stresses and their impact on organisms, particularly on animals, more relaxed, more scientifically based and without personal bias.
In ecological terms, stress may be defined as any internal state in an organism resulting from placing it outside its fundamental ecological niche, whereby the niche may be defined in terms of gene expression profiles under normal or ideal operating conditions [1]. This definition implies that stress is something that happens to organisms, something that is fate and cannot usually be avoided (if the organisms cannot escape the situation), and something that must be tolerated instead. Instead, it appears that stress in the environment, below the catastrophic or mutation threshold, is essential for individual integrity and many subtle manifestations of population structures and biodiversity, and has played a substantial role in the evolution of life. Therefore, this editorial will review highlights of environmental stresses as ecological and evolutionary driving forces and stimulate corresponding future studies.

The Individual Level

What does the “crazy worm” Caenorhabditis elegans tell us, who migrated actively into a stressful environment and suffered from stress [2]? According to current (eco)-toxicological paradigms, he must be crazy or masochistic. However, the worm does not know these paradigms and demonstrates instead that our knowledge is incomplete. In fact, several detailed studies with C. elegans revealed that the worm is by no means crazy, because he increased his Darwinian fitness [3]. Currently, it is being accepted that mild oxidative stress is mandatory for individual fitness and development. Again with C. elegans, it has recently been shown [4] that the reduction of the oxidative stress in mitochondria by adding antioxidants, significantly impaired the fitness of the nematodes. Oxidative stress in the mitochondria is central to promote longevity and reproduction [4,5].
Gene expression gives the first indication of cellular response potentials. Yet, such molecular biological data should be combined with further “omics” techniques, since the production of mRNA does not necessarily lead to corresponding proteins. Supplementation by proteomics or metabolomics is necessary, since these approaches indicate prevailing defense pathways. This indicates not all stress response lies in the genes. The translation of transcription products into proteins can be strongly modulated by several epigenetic mechanisms [6,7] or the action of microRNAs. MicroRNAs, an abundant class of newly identified endogenous non-protein-coding RNAs, have long been considered as “junk RNA”. Only recently the paradigm shifted completely, and these RNAs are now considered major regulatory tools [8], particularly in response to abiotic as well as biotic stresses as shown especially with plants. But even more striking, they have the power of cross-kingdom regulation, plant microRNAs do not lose their properties if they pass the gut of consuming animals, instead they stay intact, cross the epithelium, and display regulatory functions in the animals different from those in plants [9].

The Population and Community Level

The last examples shows that stress defense can be passed through different trophic levels. Similar phenomena, based on plant secondary metabolites, are well understood and termed “xenohormesis”. These plant molecules interact with and modulate key regulators of the physiology of animals and fungi in ways that are beneficial to health [10]. These cues provide advance warning about deteriorating environmental conditions, allowing animals and fungi to prepare for adversity while conditions are still favorable. So far, only plant secondary metabolites are discussed in terms of xenohormesis. Yet, one may speculate that microRNAs may be as significant as or even more important than the secondary metabolites.
The acquisition of stress resistance by feeding plants is, however, not the only way how populations or communities benefit from being stressed by environmental challenges. For instances, one stressor prepares the subject for the next one to come. Natural xenobiotics in the environment can induce a broad resistance to a variety of abiotic as well as biotic stressors [11]. It is not hard to assume that this phenomenon of cross-tolerance is much more wide-spread than currently documented. Since multiple stress resistance can be passed to succeeding generations by epigenetic mechanisms [12,13], this mechanism facilitates the persistence of populations in fluctuating environments. Later in calmer environments, the epigenetic markers get lost and the energy consuming mechanisms of stress defense are no longer active.
As in the aging human society and limited resources such as jobs, also stressed environmental populations have to face demographic problems with an intrinsic risk of extinction, because mild stress can produce extended individual life spans, but decreased offspring numbers.

Environmental Stresses: Ecological Driving Force and Key Player of Evolution

Natural environment have always been hostile for organisms. Exposure to climatic stress is the norm in nature, and hydrological changes, especially drought and flood, are of major importance. Human interference can exacerbate these effects [14]. Consequently, environmental stress is notoriously associated with population decline and extinction; hence, it’s potentially positive roles in shaping communities and triggering evolution are often overlooked, and if considered, they are often still gene-centered. However, clearly below the mutation threshold and even below the epigenetically triggered inheritance of acquired properties, environmental stresses are essential driving forces in ecosystems which enable life particularly in fluctuating environments. At an even more fundamental level, it is clear that environmental stressors have been and still are key players in shaping organismal evolution. In other words, moderate stress plays an important role in facilitating local adaptation by enabling better adjustments, synchronization, and functioning of many organismal systems. On the other hand, response to an acute and unfamiliar stressor precludes normal organismal functions, and the high cost of stress tolerance or lack of evolved stress response strategies leads to evolutionary stasis [15].
There is a growing body of empirical evidence that environmental stressors promote micro evolution, that is the change of gene frequency within a population over time. Arguably, the most common mechanism for phenotypic changes, however, is mutation, since phenotypes inherited epigenetically usually exhibit rapid variation. Yet, there is increasing evidence that even particularly the HSP-mediated histone pathway of epigenetic can lead to mutationlike phenotypic changes. Large HSPs comprise a specific buffering mechanism of phenotypic variability; but environmental stress can compromise this buffer with subsequent releases of hidden variations [16]. Since most of the studies were carried out with the benzoquinone ansamycin antibiotic, geldanamycin, which specifically binds to HSP90, future studies have to show whether or not realistic environmental challenges have a comparable power to increase phenotypic variability.
In sum, not all stress is stressful; and biologists can discover a variety of fascinating stress-related phenomena and thereby overcome outdated paradigms of environmental biology.


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