Once mercury enters the water system, it is converted by microorganisms into organic forms, such as methylmercury and dimethylmercury. Highly toxic organic forms of mercury with bioavailable properties are ingested by all kinds of organisms, thus being transferred through all the links in the food chain ^[9][30]. Ingested Hg persists in the body and bioaccumulates, so larger organisms tend to accumulate higher amounts of this element. This effect happens because their diet is based on an intake of a large number of smaller organisms, which have previously ingested Hg. For this reason, the consumption of large marine organisms, such as tuna or swordfish, can lead to health problems in the human population and in different animal species because they tend to accumulate greater amounts of Hg ^[9][30]. The consumption of marine organisms is the primary source of human MeHg exposure ^[22][8]. The bioconcentration of MeHg in phytoplankton and zooplankton can be as high as 10⁵ and 10⁶ times compared to MeHg concentrations in seawater, respectively ^[22][8]. Intracellular MeHg is later bound to proteins of phytoplankton cells and further bioaccumulated in marine food webs. Thus, as a primary entry point of Hg into aquatic food webs, algae play an important role in the intake and transformation of Hg species in aquatic ecosystems ^[23][83].

When MeHg enters the human body, the enterohepatic cycle is unable to expel it, so it is retained and substantially increases its half-life in the body ^[21][16]. The hydrophobic properties of MeHg allow it to pass the blood–brain barrier and even enter the placenta. MeHg interacts directly with both cellular and nuclear components, causing neurotoxic effects in the brain and nervous system, damaging the kidneys, and causing irreparable damage to fetuses ^[21][24][16,84].

Legislation regarding Hg limits in the environment and food varies by state and the environmental matrix considered. The Minamata Convention on mercury does not establish specific environmental limits, but it obliges to control and reduce Hg emissions and release globally ^[25][85]. The WHO (World Health Organization) raises awareness of Hg toxicity and exposure risks for the general population and gives an example of documented central nervous system damage in subjects exposed to 20 µg/m³ Hg in air for several years ^[26][86]. European Commission Directive 2008/105/EC (of the European Union) establishes environmental quality standards for water to protect aquatic organisms and ecosystems and limits Hg content to 20 ng/L in surface water ^[27][87]. The EU also has several additional regulations related to Hg, the most recent being European Commission Directive 2023/915/EC, establishing maximum levels of Hg at 1 mg/kg for fish ^[28][88].

The MeHg ion (CH₃Hg⁺) has a great affinity for organic and inorganic sulfuric compounds, such as sulfides and thiols, the presence of which causes MeHg speciation, giving it hydrophobic properties and increasing its bioavailability ^[24][29][68,84]. For example, it has been observed that the MeHg complex with cysteine behaves as a mobile nutrient that is actively transported to the endosperm of rice grains and that the concentration of thiols can both promote and inhibit the methylation of IHg by anaerobic bacteria ^[24][29][68,84]. Generally, the methylation rate may be affected by a specific strain of bacteria and chemical structure and concentration of organic ligand and thiol compounds ^[30][89].

Photosynthetic marine microorganisms (phytoplankton) carry out half of the global CO₂ sequestration while generating half of the O₂, which is equivalent to 1% of the global biomass of plants ^[31][90]. For this reason, they play a key role both in regulating the planet’s biogeochemical cycles (especially carbon cycles), as well as in the global ecosystem and climate change ^[31][32][90,91]. The great capacity of phytoplankton to fix CO₂ can be very useful in the future, enabling the design of CO₂ capture systems based on microalgae, as they need much less space and resources, in addition to fixing CO₂ with an efficiency between 10 and 50 times higher than other photosynthetic organisms ^[32][33][91,92]. Furthermore, the possibility of the utilization of microalgae as a food source is becoming of greater interest since they do not compete with terrestrial crops for agricultural land ^[34][93].

Phytoplankton encompasses the free-floating photosynthetic microorganisms present in the top layer of natural waters, namely, eukaryotic algae and cyanobacteria ^[35][94]. By photosynthetic biomass production, microalgae influence the composition and productivity of communities of all higher organisms ^[35][94]. To perform photosynthesis, microalgae take up nutrients from their environment, including trace metals ^[35][94]. This greatly influences the biogeochemical cycling of these elements, as metals accumulated by phytoplankton will be further transferred to other microbial communities and grazers ^[35][94]. Microalgae can be affected by various pollutants present in aquatic ecosystems ^[36][95]. Heavy metals constitute important environmental pollutants because of their potent metabolic toxicity for organisms ^[37][96]. Heavy metals like mercury may accumulate in primary producers, such as microalgae, and, ultimately, be transferred to other trophic levels ^[38][22].

There is substantial evidence that exposure to both IHg and MeHg induces general toxic effects in primary producers, including a reduction in growth and photosynthesis, as well as oxidative stress ^[35][36][39][10,94,95]. In turn, these negative effects inhibit their development and reproduction by causing physiological and metabolic irregularities ^[40][97]. Fortunately, it is established that the concentrations of Hg typically found in water are far below the amounts that significantly affect the photosynthesis and growth of microalgae ^[41][98].

However, mercury is distinguished from other heavy metals due to its tendency to bioaccumulate along entire aquatic food webs ^[42][99]. Mercury has a specific interaction with sulfhydryl groups in enzymes, and coupled with oxidative stress caused by its exposure, mercury can exert toxicity at all trophic levels ^[42][99]. Once inside algal cells, Hg may bind to cytosolic ligands and be distributed into organelles. The principle of Hg toxicity is blocking functional groups of enzymes by either displacing the ions from these sites or by modifying their conformation ^[35][94].

Hg^II was proven to be highly toxic to the photosynthetic system of microalgae by affecting the electron transport chain, changing the photochemistry of photosystem II, and, ultimately, lowering the quantum yield of photosynthesis ^[36][95]. Moreover, excessive reactive oxygen species (ROS) caused by Hg^II exposure can cause detrimental effects on gene expression and, all in all, cellular damage ^[36][95]. Some studies have shown that at low concentrations, MeHg may not have a significant effect on the electron transport chain but rather affects the metabolism of organelles in the cytoplasm and, consequently, membrane integrity, while IHg directly affects plasma membrane integrity ^[39][10]. Certain studies have also found that genes involved in cell motility, nutrition, and amino acid metabolism of the alga Chlamydomonas reindhartii were downregulated even under environmental concentrations of Hg (10⁻¹¹–10⁻⁸ M) ^[36][95].

The intake of metals in phytoplankton cells results from passive (diffusion and adsorption) and active uptake mechanisms (complexation of dissolved metals) and is driven by bioavailability conditioned by metal speciation and abundance ^[43][100]. Hg^II and MeHg are present in the environment in different forms, which fundamentally affect their bioavailability and toxicity for microalgae ^[39][10]. The impact of dissolved organic matter (DOM) is hard to predict, as in the previous studies, both increased and decreased Hg uptake by microalgae was detected. The key factors influencing this process were the concentration and composition of DOM, as well as microalgae species ^[44][73]. Higher Hg^II exposure concentrations further lead to higher cell uptake ^[36][95].

Both plants and animals have developed defense mechanisms to fight against mercury exposure, including phytoplankton ^[42][99]. Microalgae alleviate mercury toxicity by employing at least three intracellular or extracellular strategies ^[42][45][76,99] and by the increased production of antioxidants ^[46][101]. The first strategy is metal exclusion by reducing the metal-reactive cell surface with fewer ligands to limit metal accumulation ^[35][45][76,94]. The immobilization of Hg on the cell surface can significantly reduce metal toxicity. Some sources state that up to 56% of total accumulated cellular mercury can be stored in cellular debris fractions ^[42][99]. The second strategy is cellular mercury vaporization by reduction to dissolved gaseous Hg⁰, which is a less bioavailable form ^[42][45][76,99]. However, this strategy takes place only in some algae species and the detailed mechanism still seems to be unknown. The reduction of Hg has a very rapid onset and generally depends on the duration of the exposure ^[35][94]. The third strategy is to employ intracellular sulfur-rich complexes to sequester present Hg and, thus, to control its intracellular speciation and to allow separation into vacuoles ^[35][45][46][76,94,101]. The sequestration of mercury by the production of metal-binding thiol peptides is important to resist high plasmatic Hg concentrations and to restore the function of enzymes inactivated by Hg ^[42][99]. The primary species of such thiol-rich peptides found in phytoplankton are phytochelatins. Phytochelatins are produced as a response to the presence of various metals, like Cd, Cu, Pb, Ag, Zn, or Hg, in plants, algae, or yeast with a general structure of (γ-Glu-Cys)_n-Gly (n = 2–11) ^[42][99]. Phytochelatins are synthesized by the enzyme phytochelatin synthase, with glutathione as the main precursor; however, the contribution of phytochelatins to metal detoxification is specific to each metal and algal species. The differences may further include the enzymatic synthesis of phytochelatins and the stoichiometry of binding to metals ^[42][99]. The precursor of phytochelatins, glutathione, is the main non-protein thiol, the pool of which is involved in metal sequestration as well as in the mitigation of oxidative damage in cells ^[42][99]. In the event of mercury exposure, the glutathione concentration in the cell is increased and phytochelatin synthesis is induced ^[35][94]. Both glutathione and phytochelatins are able to bind cytosolic Hg and, thus, minimize its nonspecific binding to physiologically important biomolecules; however, phytochelatins have a higher capacity to bind Hg species than glutathione ^[47][102]. Besides its role in the detoxification of some xenobiotics and metals, glutathione is employed in various metabolic processes, such as the transfer and storage of reduced sulfur and the control of oxidative stress.

The excretion of accumulated Hg seems to be a problematic detoxification mechanism because of the strong intracellular binding of Hg ^[35][94]. Furthermore, MeHg seems to be a poor inducer of phytochelatins ^[35][94].