diclofenac from water per gram of algal biomass, although no live microalgal
biomass was used as a comparison.
Microalgal biodegradation involves the transformation or breakdown of complex
compounds into simpler molecules either through direct catalytic metabolic degradation, in which the compound serves as the carbon source or electron donor/
acceptor, or by co-metabolism, in which the compound is degraded by enzymes
that are catalyzing other substrates present [2]. Microalgal biodegradation can occur
either intracellularly, where the compound is taken up by the cell; extracellularly,
where enzymes are excreted into the EPS to function as an external digestive system;
or a combination of them. The intracellular biodegradation of compounds involves a
complex enzymatic process involving both Phase I and Phase II enzyme families.
The main role of Phase I enzymes in biodegradation is to make the compound more
hydrophilic, while the main role of Phase II enzymes is to catalyze the degradation of
the compound [42]. Microalgal-mediated biodegradation is regarded as being highly
complex, and the exact role of the multiple enzymes in both the Phase I and Phase II
enzyme families is not fully understood [42], and both the enzymes involved and
their respective roles are likely to differ, at least in part, between different microalgal
species [2].
There are few studies that have assessed microalgal biodegradation of a limited
number of NSAID compounds, and despite NSAIDs being hydrophilic, the reported
rates of microalgal-mediated biodegradation are low. For example, reported
microalgal biodegradation rates of the NSAID diclofenac range from <7% to 22%
and require at least a 9-day exposure to microalgal culture [44, 45]. However, the
authors did not state whether the microalgal culture was axenic or not, or if any
associated bacteria could have played a role in the reported degradation. Similarly,
Ding et al. [46] found varying rates of degradation of the NSAID naproxen between
different microalgal species, with Cymbella sp. enhancing naproxen degradation by
27% above that in the control while Scenedesmus quadricauda inhibiting degradation by 23%, following 30 days of incubation. One of the challenges to successful
microalgal biodegradation of NSAIDs is ensuring that the microalgae can uptake the
hydrophilic compounds into the cell in the first place or that extracellular enzymes
are expressed in sufficient quantity to induce extracellular degradation. Fungal
biodegradation of NSAIDs has been attributed to extracellular ligninolytic enzymes
(e.g., peroxidases, laccases), often in coordination with an internal detoxification
process, involving both Phase I and Phase II enzymes, which is mediated by the
cytochrome P450 family (CYP), epoxidases, and transferases [47, 48]. These
enzymes have also been reported as being present, to some degree, in some
microalgae, but their efficacy and mode of action (redox mediator) may vary, and
the exact role these enzymes play in microalgal biodegradation of compounds is
unknown [42, 48–50]. There are several strategies that may potentially improve
microalgal-mediated biodegradation of NSAIDs. Firstly, the conditions of the
growth media can be optimized to enhance the secretion, activity, and stability of
native laccases; for instance, Otto et al. found increased laccase production in
microalgae was achieved through the simple addition of copper sulfate. Secondly,
the catalytic performance of the native enzymes can be increased by random
224
L. N. Nguyen et al.
biomass was used as a comparison.
Microalgal biodegradation involves the transformation or breakdown of complex
compounds into simpler molecules either through direct catalytic metabolic degradation, in which the compound serves as the carbon source or electron donor/
acceptor, or by co-metabolism, in which the compound is degraded by enzymes
that are catalyzing other substrates present [2]. Microalgal biodegradation can occur
either intracellularly, where the compound is taken up by the cell; extracellularly,
where enzymes are excreted into the EPS to function as an external digestive system;
or a combination of them. The intracellular biodegradation of compounds involves a
complex enzymatic process involving both Phase I and Phase II enzyme families.
The main role of Phase I enzymes in biodegradation is to make the compound more
hydrophilic, while the main role of Phase II enzymes is to catalyze the degradation of
the compound [42]. Microalgal-mediated biodegradation is regarded as being highly
complex, and the exact role of the multiple enzymes in both the Phase I and Phase II
enzyme families is not fully understood [42], and both the enzymes involved and
their respective roles are likely to differ, at least in part, between different microalgal
species [2].
There are few studies that have assessed microalgal biodegradation of a limited
number of NSAID compounds, and despite NSAIDs being hydrophilic, the reported
rates of microalgal-mediated biodegradation are low. For example, reported
microalgal biodegradation rates of the NSAID diclofenac range from <7% to 22%
and require at least a 9-day exposure to microalgal culture [44, 45]. However, the
authors did not state whether the microalgal culture was axenic or not, or if any
associated bacteria could have played a role in the reported degradation. Similarly,
Ding et al. [46] found varying rates of degradation of the NSAID naproxen between
different microalgal species, with Cymbella sp. enhancing naproxen degradation by
27% above that in the control while Scenedesmus quadricauda inhibiting degradation by 23%, following 30 days of incubation. One of the challenges to successful
microalgal biodegradation of NSAIDs is ensuring that the microalgae can uptake the
hydrophilic compounds into the cell in the first place or that extracellular enzymes
are expressed in sufficient quantity to induce extracellular degradation. Fungal
biodegradation of NSAIDs has been attributed to extracellular ligninolytic enzymes
(e.g., peroxidases, laccases), often in coordination with an internal detoxification
process, involving both Phase I and Phase II enzymes, which is mediated by the
cytochrome P450 family (CYP), epoxidases, and transferases [47, 48]. These
enzymes have also been reported as being present, to some degree, in some
microalgae, but their efficacy and mode of action (redox mediator) may vary, and
the exact role these enzymes play in microalgal biodegradation of compounds is
unknown [42, 48–50]. There are several strategies that may potentially improve
microalgal-mediated biodegradation of NSAIDs. Firstly, the conditions of the
growth media can be optimized to enhance the secretion, activity, and stability of
native laccases; for instance, Otto et al. found increased laccase production in
microalgae was achieved through the simple addition of copper sulfate. Secondly,
the catalytic performance of the native enzymes can be increased by random
224
L. N. Nguyen et al.