The toxicity of cadmium (Cd) as a priority pollutant has been widely recognized, and much attention has been paid to the interaction between Cd and organisms. The Cd speciation and organism physiology could be greatly influenced by environmental and biological factors, leading to differential Cd toxicity. Historically, attempts have been made to adopt the free ion activity model (FIAM) to explain and predict Cd toxicity, but the conclusions are far from consistent. And currently there is no specific biotic ligand model (BLM) for Cd to predict its toxicity in aquatic organisms. More recently, a new model, namely, the subcellular partitioning model (SPM), has been proposed as a more mechanistic method to understand metal toxicity. However, the applicability of SPM in Cd toxicity explanati...[
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The toxicity of cadmium (Cd) as a priority pollutant has been widely recognized, and much attention has been paid to the interaction between Cd and organisms. The Cd speciation and organism physiology could be greatly influenced by environmental and biological factors, leading to differential Cd toxicity. Historically, attempts have been made to adopt the free ion activity model (FIAM) to explain and predict Cd toxicity, but the conclusions are far from consistent. And currently there is no specific biotic ligand model (BLM) for Cd to predict its toxicity in aquatic organisms. More recently, a new model, namely, the subcellular partitioning model (SPM), has been proposed as a more mechanistic method to understand metal toxicity. However, the applicability of SPM in Cd toxicity explanation and prediction as well as the importance of phytochelatins in Cd detoxification are not well known for marine phytoplankton. Therefore, a series of experiments were conducted to investigate differential Cd toxicity, using Cd accumulation, subcellular distribution and phytochelatin (PC) synthesis as major tools. These included Cd toxicity experiments under different irradiance and temperature conditions, after exposure to and recovery from different levels of environmental Cd stress for various durations for a Hong Kong local marine diatom Thalassiosira nordenskioeldii. Another experiment investigating the species differential Cd sensitivity was also conducted for the marine diatom Thalassiosira pseudonana, green algae Chlorella autotrophica, and dinoflagellate Prorocentrum minimum.
Generally, increased irradiance and temperature led to an elevation in Cd sensitivity by exerting great influence on the diatom’s biochemical composition (e.g., C/N ratio and phytochelatin and related peptides synthesis) and physiological processes (e.g. the growth rate, photosynthesis, Cd uptake, accumulation and subcellular distribution). However, the calculated median inhibition concentration (IC50) based on MSF-Cd (Cd concentration in metal sensitive fraction) or organelle-Cd exhibited the least difference, strongly meriting MSF-Cd and organelle-Cd being the best indicators of Cd toxicity for marine diatom at different environmental conditions. A similar result was also obtained for the species differential Cd sensitivity experiment. Therefore, the subcellular partitioning model, which incorporates the subcellular fates of metal, may provide a better means to predict metal toxicity as compared to the FIAM or the BLM.
Exposure history also exerted great influence on the subsequent Cd sensitivity. The Cd sensitivity increased with the pre-exposed [Cd
2+] and period, due to the physical accumulation of Cd concentration in MSF and the possible functional damage on MSF. After the environmental Cd stress was alleviated, the Cd sensitivity initially increased followed by a gradual restoration, the extent of which depending on the pre-exposed [Cd
2+] and recovery period. Irreversible toxic effects on the diatoms during the exposure period may prevent a further and complete restoration of Cd tolerance even after long time of recovery.
The intracellular PC pool was tightly and dynamically controlled by the cell. Therefore the responses of PCs were quick not only to the elevation of environmental [Cd
2+], but also to the alleviation of [Cd
2+] stress. When putting together the data obtained from different Cd toxicity experiments for T. nordenskioeldii (under different temperature condition, after Cd exposure and recovery), a strong relationship between [Cd
2+] or intra-Cd and the relative change in PC-SH was observed, providing a strong and quantitative support of the role of PC-SH in phytoplankton as a good indicator of environmental and intracellular Cd stress. The intra-Cd/PC-SH ratio (or intra-Cd to PC-SH difference), however, could not always explain the differential Cd toxicity as expected. The possible reasons included other detoxification mechanisms, the turnover of PCs and the function of PCs other than detoxification.
In conclusion, the subcellular partitioning model is more accurate and mechanistic in Cd toxicity explanation and prediction compared to FIAM and BLM. Additionally, the phytochelatin showed its potential as a good bioindicator of environmental and cellular Cd stress. However, Cd detoxification pathways other than PC and the turnover of PC need further investigation for better understanding of Cd toxicity and detoxification in marine phytoplankton.
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