scholarly journals The price of defence: toxins, visual signals and oxidative state in an aposematic butterfly

2021 ◽  
Author(s):  
Jonathan D Blount ◽  
Hannah M Rowland ◽  
Christopher Mitchell ◽  
Michael P Speed ◽  
Graeme D Ruxton ◽  
...  

In a variety of aposematic species, the conspicuousness of an individual's warning signal and the quantity of its chemical defence are positively correlated. This apparent honest signalling in aposematism is predicted by resource competition models which assume that the production and maintenance of aposematic defences compete for access to antioxidant molecules that have dual functions as pigments directly responsible for colouration and in protecting against oxidative lipid damage. Here we study a model aposematic system - the monarch butterfly (Danaus plexippus) and make use of the variable phytochemistry of its larval host-plant, milkweeds (Asclepiadaceae), to manipulate the concentration of sequestered cardenolides. We test two fundamental assumptions of resource competition models: that (1) the possession of secondary defences is associated with costs in the form of oxidative lipid damage and reduced antioxidant defences; and (2) that oxidative damage or decreases in antioxidant defences can reduce the capacity of individuals to produce aposematic displays. Monarch caterpillars that sequestered the highest concentrations of cardenolides exhibited higher levels of oxidative lipid damage as adults. The relationship between warning signals, cardenolide concentrations and oxidative damage differed between the sexes. In male monarchs conspicuousness was explained by an interaction between oxidative damage and sequestration: as males sequester more cardenolides, those with high levels of oxidative damage become less conspicuous, while those that sequester lower levels of cardenolides equally invest in conspicuous with increasing oxidative damage. There was no significant effect of oxidative damage or concentration of sequestered cardenolides on female conspicuousness. Our results demonstrate physiological linkage between the production of coloration and protection from autotoxicity, that warning signals can be honest indicators of defensive capability, and that the relationships are different between the sexes.

2002 ◽  
Vol 61 (2) ◽  
pp. 191-202 ◽  
Author(s):  
Michael Grundman ◽  
Patrick Delaney

Oxidative damage is present within the brains of patients with Alzheimer's disease (AD), and is observed within every class of biomolecule, including nucleic acids, proteins, lipids and carbohydrates. Oxidative injury may develop secondary to excessive oxidative stress resulting from β-amyloid-induced free radicals, mitochondrial abnormalities, inadequate energy supply, inflammation or altered antioxidant defences. Treatment with antioxidants is a promising approach for slowing disease progression to the extent that oxidative damage may be responsible for the cognitive and functional decline observed in AD. Although not a uniformly consistent observation, a number of epidemiological studies have found a link between antioxidant intake and a reduced incidence of dementia, AD and cognitive decline in elderly populations. In AD clinical trials molecules with antioxidant properties such as vitamin E andGinkgo bilobaextract have shown modest benefit. A clinical trial with vitamin E is currently ongoing to determine if it can delay progression to AD in individuals with mild cognitive impairment. Combinations of antioxidants might be of even greater potential benefit for AD, especially if the agents worked in different cellular compartments or had complementary activity (e.g. vitamins E, C and ubiquinone). Naturally-occurring compounds with antioxidant capacity are available and widely marketed (e.g. vitamin C, ubiquinone, lipoic acid, β-carotene, creatine, melatonin, curcumin) and synthetic compounds are under development by industry. Nevertheless, the clinical value of these agents for AD prevention and treatment is ambiguous, and will remain so until properly designed human trials have been performed.


2006 ◽  
Vol 17 (10) ◽  
pp. 665-671 ◽  
Author(s):  
P TAULER ◽  
A SUREDA ◽  
N CASES ◽  
A AGUILO ◽  
J RODRIGUEZMARROYO ◽  
...  

2009 ◽  
Vol 29 (9) ◽  
pp. 1187-1198 ◽  
Author(s):  
J. C. Melgar ◽  
L. Guidi ◽  
D. Remorini ◽  
G. Agati ◽  
E. Degl'innocenti ◽  
...  

2005 ◽  
Vol 2 (1) ◽  
pp. 45-52 ◽  
Author(s):  
B. L. Gros ◽  
D. S. Greenhouse ◽  
T. E. Cohn

This study aimed to answer the question of how to design a visual warning signal that is most easily seen and produces the quickest reaction time. This is a classic problem of bionic optimization—if one knows the properties of the receiver one can most easily find a suitable solution. Because the peak of the spatio-temporal contrast sensitivity function of the human visual system occurs at non-zero spatial and temporal frequencies, it is likely that movement enhances the detectability of threshold visual signals. Earlier studies employing extended drifting sinewave gratings bear out this prediction. We have studied the ability of human observers to detect threshold visual signals for both moving and stationary stimuli. We used discrete, localized signals such as might be employed in aerospace or automotive warning signal displays. Moving stimuli show a superior detectability to non-moving stimuli of the same integrated energy. Moving stimuli at threshold detectability are seen faster than non-moving threshold stimuli. Under some conditions the speed advantage is over 0.25 seconds. Similar advantages have also been shown to occur for suprathreshold signals.


1998 ◽  
Vol 94 (4) ◽  
pp. 447-452 ◽  
Author(s):  
E. García-Arumí ◽  
A. L. Andreu ◽  
J. López-Hellín ◽  
S. Schwartz

1. Oxidative damage has been associated with ageing, but there is no agreement as to whether or not it is produced by a decrease in antioxidant defences with the ageing process. In purified lymphocytes from 47 healthy elderly (75.27 ± 0.91 years) and 47 healthy young (29.87 ± 0.53 years) volunteers, we studied the levels of antioxidant enzyme activity (superoxide dismutase, catalase and glutathione peroxidase), protein oxidative damage (as protein carbonyl content) and lysosomal proteolytic activity (cathepsins B, H and L), with and without exposure to oxidative stress produced by 25 μmol/l H2O2. 2. There were no differences in antioxidant enzyme activities in the stressed and non-stressed samples between the young and elderly subjects, indicating that there was no relationship between age and antioxidant enzyme activity even in oxidative stress. However, a dissimilar response to oxidative stress was observed in protein oxidative damage and cathepsin B and L activities, depending on the age of the donor. 3. With these results we conclude that oxidative stress produces greater protein oxidative damage and increased protein degradation in elderly subjects than in young ones; this effect cannot be attributed to dissimilar antioxidant enzyme responses to oxidative stress, since these did not differ between the two age groups.


2011 ◽  
Vol 56 (No. 11) ◽  
pp. 537-546 ◽  
Author(s):  
M. Sevcikova ◽  
H. Modra ◽  
A. Slaninova ◽  
Z. Svobodova

This review summarizes the current knowledge on the contribution of metals to the development of oxidative stress in fish. Metals are important inducers of oxidative stress in aquatic organisms, promoting formation of reactive oxygen species through two mechanisms. Redox active metals generate reactive oxygen species through redox cycling, while metals without redox potential impair antioxidant defences, especially that of thiol-containing antioxidants and enzymes. Elevated levels of reactive oxygen species lead to oxidative damage including lipid peroxidation, protein and DNA oxidation, and enzyme inactivation. Antioxidant defences include the enzyme system and low molecular weight antioxidants. Metal-binding proteins, such as ferritin, ceruloplasmin and metallothioneins, have special functions in the detoxification of toxic metals and also play a role in the metabolism and homeostasis of essential metals. Recent studies of metallothioneins as biomarkers indicate that quantitative analysis of mRNA expression of metallothionein genes can be appropriate in cases with elevated levels of metals and no evidence of oxidative damage in fish tissue. Components of the antioxidant defence are used as biochemical markers of oxidative stress. These markers may be manifested differently in the field than in results found in laboratory studies. A complex approach should be taken in field studies of metal contamination of the aquatic environment.  


2014 ◽  
Vol 65 (1) ◽  
pp. 37-46 ◽  
Author(s):  
Jelena Mladenović ◽  
Branka Ognjanović ◽  
Nataša Đorđević ◽  
Miloš Matić ◽  
Veroljub Knežević ◽  
...  

Summary The aim of this study was to investigate the protective effects of oestradiol (E2, 4 mg kg-1 b.w. i.p.) against cadmium-induced (Cd, 2 mg kg-1 b.w. i.p.) blood changes in rats. Cadmium induced a significant decline in haemoglobin, haematocrit, and total erythrocyte, lymphocyte, and thrombocyte count, whereas total leukocytes and granulocytes increased. A significant increase was also observed in serum cholesterol, triglycerides, glucose, AST, and ALT activities, whereas total protein and albumin levels dropped significantly. Administration of E2 in combination with Cd alleviated most of these adverse effects. In terms of oxidative stress, Cd significantly increased oxygen-free radicals (O2 •- and H2O2) in neutrophils and lipid peroxidation in erythrocytes, whereas E2 treatment reversed these changes to control values. Acute Cd poisoning significantly lowered antioxidant enzyme (SOD and CAT) activity and the level of non-enzymatic antioxidants (GSH and vitamin E), while increasing in GSSG. Treatments with E2 reversed Cd-induced effects on the antioxidant defences and significantly lowered Cd-induced oxidative damage in erythrocytes. This study suggests that exogenous E2 effectively restores redox balance in rat erythrocytes and counters adverse haematological and biochemical effects of Cd poisoning. It also improves the antioxidant capacity of erythrocytes, acting in synergy with endogenous antioxidants.


2021 ◽  
Author(s):  
Ruchuan He ◽  
Craig Barnett ◽  
Emilio Pagani-Núñez ◽  
Eben Goodale

Abstract Aposematic organisms defend themselves through various means to increase their unprofitability to predators which they advertise with conspicuous warning signals. Predators learn to avoid aposematic prey through associative learning that leads to lower predation. However, when these visual signals become unreliable (e.g., through automimicry or Batesian mimicry), predators may switch from using visual signals to taste sampling prey to choose among them (‘go-slow’ behaviour). In this experiment, we tested this possibility in a field experiment where we released a total of 9600 mealworm prey of two types: (i) undefended prey (injected with water) and (ii) model-mimics (injected with either quinine sulphate [models] or water [mimics]). Prey were deployed at 12 sites, each with a mimic frequency ratio between 0 to 1, at 0.2 intervals. We found that taste rejection peaked at moderate mimic frequencies (0.4 and 0.6), supporting the idea that taste sampling and rejection of prey is related to signal reliability and predator uncertainty. This is the first time that taste-rejection has been shown to be related to the reliability of prey signals in a mimetic prey system.


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