Many algae have immense capability to sorb metals, and there is considerable potential for using them to treat wastewaters. Metal sorption involves binding on the cell surface and to intracellular ligands. The adsorbed metal is several times greater than intracellular metal. Carboxyl group is most important for metal binding. Concentration of metal and biomass in solution, pH, temperature, cations, anions and metabolic stage of the organism affect metal sorption. Algae can effectively remove metals from multi-metal solutions. Dead cells sorb more metal than live cells. Various pretreatments enhance metal sorption capacity of algae. CaCl2 pretreatment is the most suitable and economic method for activation of algal biomass. Algal periphyton has great potential for removing metals from wastewaters. An immobilized or granulated biomass-filled column can be used for several sorption/desorption cycles with unaltered or slightly decreased metal removal. Langmuir and Freundlich models, commonly used for fitting sorption data, cannot precisely describe metal sorption since they ignore the effect of pH, biomass concentration, etc. For commercial application of algal technology for metal removal from wastewaters, emphasis should be given to: (i) selection of strains with high metal sorption capacity, (ii) adequate understanding of sorption mechanisms, (iii) development of low-cost methods for cell immobilization, (iv) development of better models for predicting metal sorption, (v) genetic manipulation of algae for increased number of surface groups or over expression of metal binding proteins, and (vi) economic feasibility.

Summary 1. All heavy metals, including those that are essential micronutrients (e.g. copper, zinc, etc.), are toxic to algae at high concentrations. 2. One characteristic feature of heavy‐metal toxicity is the poisoning and inactivation of enzyme systems. Many of the physiological and biochemical processes, viz., photosynthesis, respiration, protein synthesis and chlorophyll synthesis, etc., are severely affected at high metal concentrations. 3. Some algae inhabit waters chronically polluted with heavy‐metal‐laden wastes from mining and smelting operations; Nodularia sp., Oscillatoria sp., Cladophora sp., Hormidium sp., Fucus sp. and Laminaria sp., etc., occur in metal‐rich waters. These algal forms are probably more capable of combating the toxic levels of heavy metals and this attribute is a result of physiological and/or genetic adaptations. The sensitivity or tolerance to heavy metals varies amongst different algae. The phenomena of multiple tolerance and co‐tolerance may be exhibited by some algae. 4. Heavy‐metal pollution causes reduction in species diversity leading to the dominance of a few tolerant algal forms. The primary productivity also decreases after metal supplementation. 5. The uptake and accumulation of heavy metals can be active (energy‐dependent), passive (energy‐independent), or both. 6. Heavy metals can be safely stored as intranuclear complexes by some algae. Notwithstanding this, some changes in the cell wall can enable the algae to tolerate heavy metals by checking the entry of the metals (exclusion mechanism). 7. The metal content of algae growing in a waterbody may yield valuable information for simulating heavy metal pollution: several species of Cladophora and Fucus have been extensively used for this purpose. 8. Several factors affect and determine toxicity of heavy metals to algae. At low pH, the availability of heavy metals to algae is greatly increased, as a consequence of which pronounced toxicity is evident. Hard waters decrease metal toxicity. Some ions, e.g., calcium, magnesium and phosphorus, can alleviate toxicity of metals. 9. The presence of other metals can influence toxicity of a heavy metal through simple additive effect or by synergistic and antagonistic interactions. Similarly, other pollutants can influence heavy‐metal toxicity. 10. The toxicity of heavy metals depends upon their chemical speciation. Various ionic forms of a metal characterized by different valency states, may be differentially toxic to a test alga. 11. Amino acids, organic matter, humic acids, fulvic acid, EDTA, NTA, etc. can complex with heavy metals and render them unavailable. This may eventually lead to less toxicity. 12. Heavy‐metal toxicity largely depends upon algal population density: the denser the population the more numerous the cellular sites available, leading to decreased toxicity.

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Exposure of Chlorella vulgaris to elevated concentrations of copper, chromium, nickel and zinc led to intracellular accumulation of high concentrations of these metals. Concomitantly, accumulation of free proline occurred, depending on the concentration of metals in the external medium or in the cell. The greater the toxicity or accumulation of a metal, the greater the amount of intracellular proline in algal cells. However, higher concentrations of copper and chromium were inhibitory to proline accumulation by the test organism. The accumulation of proline was triggered within a few hours of metal treatment. Test metals also induced lipid peroxidation ; copper was the most efficient inducer whereas zinc was the least. Pretreatment of C. vulgaris with proline counteracted metal-induced lipid peroxidation and potassium ion efflux. Thus the present work shows a protective effect of proline on metal toxicity through inhibition of lipid peroxidation.

A 4-h exposure of Scenedesmus sp. to Cu or Zn enhanced intracellular levels of both test metals and proline. The level of intracellular proline increased markedly up to 10 microM Cu, but higher concentrations were inhibitory. However, intracellular proline consistently increased with increasing concentration of Zn in the medium. Cu and Zn induced oxidative stress in the test alga by increasing lipid peroxidation and membrane permeability, and by reducing SH content. Pretreatment of the test alga with 1 mM proline for 30 min completely alleviated Cu-induced lipid peroxidation, minimized K+ efflux and also reduced depletion of the SH pool. But proline pretreatment could only slightly reduce Zn-induced oxidative stress. Interestingly, proline pretreatment increased the level of Cu (25-54%) and Zn (19-49%) inside the cells. It did not affect the activities of superoxide dismutase, ascorbate peroxidase or catalase, but improved glutathione reductase activity under Cu and Zn stress. A comparison of the effects of proline pretreatment on lipid peroxidation by Cu, Zn, methyl viologen and ultraviolet-B radiation suggests that proline protects cells from metal-induced oxidative stress by scavenging reactive oxygen species rather than by chelating metal ions. Pretreatment of cells with a known antioxidant (ascorbate) and a hydroxyl radical scavenger (sodium benzoate) considerably reduced metal-induced lipid peroxidation and proline accumulation. However, sodium benzoate had a very mild effect on Zn-induced lipid peroxidation and proline accumulation. The present study demonstrates that proline possibly acts by detoxifying reactive oxygen species, mainly hydroxyl radicals, rather than by improving the antioxidant defense system under metal stress.