No abstract

The article expands our knowledge on the variety of biodegraders of ibuprofen, one of the most frequently detected non-steroidal anti-inflammatory drugs in the environment. We studied the dynamics of ibuprofen decomposition and its relationship with the physiological status of bacteria and with additional carbon and energy sources. The involvement of cytoplasmic enzymes in ibuprofen biodegradation was confirmed. Within the tested actinobacteria, Rhodococcus cerastii IEGM 1278 was capable of complete oxidation of 100 μg/L and 100 mg/L of ibuprofen in 30 h and 144 h, respectively, in the presence of an alternative carbon source (n-hexadecane). Besides, the presence of ibuprofen induced a transition of rhodococci from single- to multicellular lifeforms, a shift to more negative zeta potential values, and a decrease in the membrane permeability. The initial steps of ibuprofen biotransformation by R. cerastii IEGM 1278 involved the formation of hydroxylated and decarboxylated derivatives with higher phytotoxicity than the parent compound (ibuprofen). The data obtained indicate potential threats of this pharmaceutical pollutant and its metabolites to biota and natural ecosystems.

Active pharmaceutical ingredients present a substantial risk when they reach the environment and drinking water sources. As a new type of dangerous pollutants with high chemical resistance and pronounced biological effects, they accumulate everywhere, often in significant concentrations (μg/L) in ecological environments, food chains, organs of farm animals and humans, and cause an intense response from the aquatic and soil microbiota. Rhodococcus spp. (Actinomycetia class), which occupy a dominant position in polluted ecosystems, stand out among other microorganisms with the greatest variety of degradable pollutants and participate in natural attenuation, are considered as active agents with high transforming and degrading impacts on pharmaceutical compounds. Many representatives of rhodococci are promising as unique sources of specific transforming enzymes, quorum quenching tools, natural products and novel antimicrobials, biosurfactants and nanostructures. The review presents the latest knowledge and current trends regarding the use of Rhodococcus spp. in the processes of pharmaceutical pollutants’ biodegradation, as well as in the fields of biocatalysis and biotechnology for the production of targeted pharmaceutical products. The current literature sources presented in the review can be helpful in future research programs aimed at promoting Rhodococcus spp. as potential biodegraders and biotransformers to control pharmaceutical pollution in the environment.

Actinomycetes of the genus Rhodococcus (class Actinomycetia) are dominant dwellers of biotopes with anthropogenic load. They serve as a natural system of primary response to xenobiotics in open ecosystems, initiate defensive responses in the presence of pollutants, and are regarded as ideal agents capable of transforming and degrading pharmaceuticals. Here, the ability of selected Rhodococcus strains to co-metabolize nonsteroidal anti-inflammatory drugs (ibuprofen, meloxicam, and naproxen) and information on the protective mechanisms of rhodococci against toxic effects of pharmaceuticals, individually or in a mixture, have been demonstrated. For the first time, R. ruber IEGM 439 provided complete decomposition of 100 mg/L meloxicam after seven days. It was shown that versatile cellular modifications occurring at the early development stages of nonspecific reactions of Rhodococcus spp. in response to separate and combined effects of the tested pharmaceuticals included changes in electrokinetic characteristics and catalase activity; transition from unicellular to multicellular life forms accompanied by pronounced morphological abnormalities; changes in the average size of vegetative cells and surface area-to-volume ratio; and the formation of linked cell assemblages. The obtained data are considered as adaptation mechanisms in rhodococci, and consequently their increased resistance to separate and combined effects of ibuprofen, meloxicam, and naproxen.

No abstract

No abstract

No abstract

No abstract