Hi Murali,
It is a tricky question given the information provided (i.e. decreasing levels of 2 biomarkers of early oxidative stress defence, 1 biomarker of oxidative damage). It is also not so easy to know what is meant by "heavy metals" as this term is not chemically defined, and also doesn't tell us whether it is about exposure to single metals, or metal mixtures...or even essential metals. Finally it also depends on the cell densities and phase of growth of the cell as well as composition of the culture/exposure media. Only taking these factors into account it would be possible to guess what might be happening within the cell. For instance, your situation might be that an essential trace metal (e.g. Cu) was absent in the culture media and causing stress and limitation to cells, and when you expose cells to it they are healthier. The exatcly opposite situation might be possible, e.g. the cells are under such huge stress when exposed to high concentrations of a transition metal, that the microalgae effectively shuts down metabolic rates, which would explain the decrease in the measured biomarkers.
A thing to keep in mind is that these parameters most likely would have biphasic responses to metal exposure, so it might be always relevant to know which metal, which parameter, which condition to understand.
There is quite some work done with freshwater (and seawater) microalga for the Biotic Ligand Model, that could give you some insights into the mechanistics of effects in your systems. Maybe it could be nice to start with some speciation models to see which metal ion might be causing the toxicity.
Hope it helped.
;)
Hi Murali
When an organism remained under metal stress, the rate of reactive oxygen species (ROS) production goes to high. As a result antioxidant system enzyme activity increases. Sometimes the active site of active site of antioxidant enzyme is occupied with metal ions that donot permit
Substrate to bind with active part of an enzyme and hence activity of an antioxidant enzyme decrease
In most cases an increases in CAT and SOD activities at lower metal concentration but reduction on activities were observed at higher concentrations of metals this might be attributed to inactivation of the enzymes by ROS or decrease in their synthesis or both.The decrease in MDA could be to the increase in the non-enzymatic antioxidants such GSH (reduced glutathione )which consider as the mother of antioxidants which reported to be elevated in chronic exposure to heavy metals.Good luck for furthere information please see our published articles in my RG
Salut Murali , excusez moi pour ce retard...
Si l'activité de la SOD, la CAT diminue dans une cellule algale cela veut dire que le statut redox est déséquilibré à cause à l'exposition aux métaux lourds,
mais en parallèle la MDA diminue aussi; MDA est le principal marqueur de la peroxydes lipidiques suite à l’exposition à un stress oxydatif. ici dans votre cas les métaux lourds n'engendrent pas une peroxydation lipidique mais provoquent une diminution de la défense antioxydante enzymatique,
On note que La SOD est la première ligne de défense contre les radicaux libres provenant de la peroxydation lipidique.
Mois personnellement j'ai pas travailler sur les métaux lourds, mais je peut vous donner une explication;
on peut suggérer que le MDA (marqueur de la peroxydation lipidique) s'élevais au premier temps lors l'exposition au métaux lourds et que l'activité de la SOD, la CAT est augmentée initialement pour catalyser la conversion de radicaux superoxydes (O2•-) en peroxyde d’hydrogène (H2O2), et en présence d'une activité suffisante de la catalase, le peroxyde d’hydrogène (H2O2) sera converti en H2O et O2 inoffensifs.
" La sur-activation des enzymes antioxydantes pourrait améliorer la résistance à un état de stress oxydatif et indique une adaptation face au stress oxydant "
Ensuite, l'activité de la SOD et de CAT a diminué suggérant que la chronicité de l'exposition ou bien l'accumulation de ces métaux lourds épuise les sources d’enzymes antioxydantes dans le temps qui sont élevées initialement pour contrebalancer le stress oxydatif.
BON COURAGE
Dear Taleb-Belkadi Ouarda Aa,
Thank you for your good explanation. I can't understand your french language, so i have converted english version your text and upload to researchgate.
If the activity of the SOD, CAT decreases in an algal cell it means that the redox status is unbalanced because of exposure to heavy metals, but in parallel the MDA also decreases; MDA is the main marker of lipid peroxides following exposure to oxidative stress. here in your case the heavy metals do not cause a lipid peroxidation but cause a decrease in enzymatic antioxidant defense, It is noted that SOD is the first line of defense against free radicals from lipid peroxidation. Month personally I do not work on heavy metals, but I can give you an explanation; it may be suggested that MDA (lipid peroxidation marker) was initially elevated in heavy metal exposure and that SOD activity initially increased CAT to catalyze the conversion of superoxide radicals (O2). -) in hydrogen peroxide (H2O2), and in the presence of sufficient catalase activity, hydrogen peroxide (H2O2) will be converted to harmless H2O and O2. "Over-activation of antioxidant enzymes could improve resistance to oxidative stress and indicate adaptation to oxidative stress" Then, the activity of SOD and CAT decreased suggesting that the chronicity of exposure or the accumulation of these heavy metals depletes the sources of antioxidant enzymes over time that are initially high to counterbalance oxidative stress.
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