**2.2. Metal toxicity effects**

After metal ingestion, this is specifically transported by lipoproteins into different body compartments (organs, blood, or other physiological structures) where they can be specifically oriented to different centers: (i) *action centers* where the toxic metal interacts with an endogen macromolecule (protein or ADN) or a certain cellular structure inducing toxic effects for all body; (ii) *metabolism centers* where the metal is processed by detoxified enzymes; (iii) *storage centers* where the metals are collected in a toxic inactive state; and (iv) *excretion centers* where the metals are disposed.

The heavy metal overload has inhibitory effects on the development of aquatic organisms (phytoplankton, zooplankton, and fish) [34, 35]. The metallic compounds could disturb the oxygen level and mollusks development, byssus formation, as well as reproductive processes. Several histological changes such as gill necrosis or fatty degeneration of the liver occur in the fish and crustaceans [36, 37]. Assessments at the cellular level enable to understand the action of toxic metals on the enzymatic metabolism and physiology of the aquatic organisms.

of organic binders increases the bioavailability of Cd in mussels and fish, by facilitating the diffusion of the hydrophobic compound in the lipid membrane. The organic compounds of metals could be more bioavailable than the ionic forms [29]. For instance, the organic mercurial compounds are lipid‐soluble and penetrate quickly the lipid membranes, increasing the

The adsorption on suspended solids affects the total concentration of metals present in water. The association between solid particles and metals is also critical for the metal uptake into organisms through food ingestion [31]. The suspended solids accumulate the insoluble metal compounds, but under certain conditions, the metal reached the interstitial water being dissolved. Heavy metal concentrations from sediments or suspended solids are much higher than in water, so a small fraction of them could be an important source for bioaccumulation in planktonic and benthic organisms [32]. The dynamics of different forms of metals in the aquatic environment is not fully understood, so new studies are required to analyze the different accumulation/bioaccumulation pathways based on dissolved or suspended metal forms.

Other studies highlighted that bioavailability of metals in bivalve mollusks depends on sediment particle size due to their filter feeding behavior. If the particles were coated with bacterial extracellular polymers or fulvic acids, the Cd, Zn, and Ag bioavailability was significantly increased. Overall, the binding of metal decreased the bioavailability of metals

After metal ingestion, this is specifically transported by lipoproteins into different body compartments (organs, blood, or other physiological structures) where they can be specifically oriented to different centers: (i) *action centers* where the toxic metal interacts with an endogen macromolecule (protein or ADN) or a certain cellular structure inducing toxic effects for all body; (ii) *metabolism centers* where the metal is processed by detoxified enzymes; (iii) *storage centers* where the metals are collected in a toxic inactive state; and (iv) *excretion centers* where

toxicity compared to mercuric chloride which is not lipid‐soluble [30].

**Figure 2.** The main control factors that influence metal bioavailability.

from the sediment [28, 33].

62 Water Quality

**2.2. Metal toxicity effects**

the metals are disposed.

The lethal effects of metals in crustaceans were induced by the inhibition of enzymes in‐ volved in cellular respiration. The histological changes observed in fish and crustaceans af‐ ter chronic exposure to metals are the result of antioxidant enzymes inhibition [38–41]. The effects on organisms' growth and development were triggered by the inhibition of enzymat‐ ic systems involved in protein synthesis and cell division. The metal type modulates the bio‐ accumulation level and enzymatic systems vulnerability generating a multitude of effects, toxic or not [42, 43].

In order to understand the interaction mechanism between the toxic metals and the aquatic organisms and how organisms answer to metal contamination, more information on bioavail‐ ability is needed [44].

At the present, many studies on the assessment of acute and chronic toxicity of metals mentioned the following parameters: survival, growth, development, reproduction, behavior, accumulation, effects on enzyme systems, etc. In **Table 1**, the values of acute (LC50) and chronic (MATC/NOEC/LOEC) toxic concentration for fish and planktonic crustaceans according to PAN Pesticide Database—Chemical Toxicity Studies on Aquatic Organisms [45] are exempli‐ fied. The studies highlighted that the toxic concentration intervals depend on the species, exposure time, age of specimens, type of toxicity test type, and laboratory conditions.


LC (EC) 50—lethal concentrations for 50% of tested organisms after 96 or 48 h; MATC—maximum acceptable toxicant concentration in aquatic systems; NOEC—no observed effect concentration; LOEC—low observed effect concentration.

**Table 1.** Literature acute and chronic toxicity values [45–47].
