37 research outputs found
Exploring Uncoupling Proteins and Antioxidant Mechanisms under Acute Cold Exposure in Brains of Fish
Exposure to fluctuating temperatures accelerates the mitochondrial respiration and increases the formation of mitochondrial reactive oxygen species (ROS) in ectothermic vertebrates including fish. To date, little is known on potential oxidative damage and on protective antioxidative defense mechanisms in the brain of fish under cold shock. In this study, the concentration of cellular protein carbonyls in brain was significantly increased by 38% within 1 h after cold exposure (from 28°C to 18°C) of zebrafish (Danio rerio). In addition, the specific activity of superoxide dismutase (SOD) and the mRNA level of catalase (CAT) were increased after cold exposure by about 60% (6 h) and by 60%â90% (1 and 24 h), respectively, while the specific glutathione content as well as the ratio of glutathione disulfide to glutathione remained constant and at a very low level. In addition, cold exposure increased the protein level of hypoxia-inducible factor (HIF) by about 50% and the mRNA level of the glucose transporter zglut3 in brain by 50%â100%. To test for an involvement of uncoupling proteins (UCPs) in the cold adaptation of zebrafish, five UCP members were annotated and identified (zucp1-5). With the exception of zucp1, the mRNA levels of the other four zucps were significantly increased after cold exposure. In addition, the mRNA levels of four of the fish homologs (zppar) of the peroxisome proliferator-activated receptor (PPAR) were increased after cold exposure. These data suggest that PPARs and UCPs are involved in the alterations observed in zebrafish brain after exposure to 18°C. The observed stimulation of the PPAR-UCP axis may help to prevent oxidative damage and to maintain metabolic balance and cellular homeostasis in the brains of ectothermic zebrafish upon cold exposure
Interaction of Temperature and Light in the Development of Freezing Tolerance in Plants
Abstract Freezing tolerance is the result of a wide range
of physical and biochemical processes, such as the induction
of antifreeze proteins, changes in membrane composition,
the accumulation of osmoprotectants, and changes
in the redox status, which allow plants to function at low
temperatures. Even in frost-tolerant species, a certain period
of growth at low but nonfreezing temperatures, known
as frost or cold hardening, is required for the development
of a high level of frost hardiness. It has long been known
that frost hardening at low temperature under low light
intensity is much less effective than under normal light
conditions; it has also been shown that elevated light
intensity at normal temperatures may partly replace the
cold-hardening period. Earlier results indicated that cold
acclimation reflects a response to a chloroplastic redox
signal while the effects of excitation pressure extend
beyond photosynthetic acclimation, influencing plant
morphology and the expression of certain nuclear genes
involved in cold acclimation. Recent results have shown
that not only are parameters closely linked to the photosynthetic
electron transport processes affected by light
during hardening at low temperature, but light may also
have an influence on the expression level of several other
cold-related genes; several cold-acclimation processes can
function efficiently only in the presence of light. The
present review provides an overview of mechanisms that
may explain how light improves the freezing tolerance of
plants during the cold-hardening period