Journal
CHEMICAL ENGINEERING JOURNAL
Volume 407, Issue -, Pages -Publisher
ELSEVIER SCIENCE SA
DOI: 10.1016/j.cej.2020.127184
Keywords
Cytostatic; Cytotoxic; Cellular resistance; Cell regulation; Polar metabolites; Topoisomerase inhibitors
Categories
Funding
- UKIERI
- SERB, DST, India
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The fate, distribution, and removal of chemotherapeutic agents in the environment largely depend on their structural orientation, environmental factors, and degree of ionization, with key knowledge gaps and challenges identified. These agents may have an accumulation effect on aquatic species and spread drug resistance via interaction with certain kinases.
Antineoplastics (anticancer agents) i.e. alkylating and non-alkylating agents, topoisomerase inhibitors etc. are classified as the contaminants of emerging concern due to growing concern about environmental health degradation. Such cytostatic agents contain a suit of functional groups (i.e. folic acid/purine/pyrimidine/nitrogen analogues), which render their complex chemistry and determine partitioning in the aquatic systems. A systematic review of the recent literature published between 2009 and 2020 has been presented to validate the hypothesis that the environmental fate, distribution, and removal aspects of chemotherapeutic agents depend largely on the structural orientation, environmental (and genetic) factors, and degree of ionization. The key knowledge gaps on the current challenges and opportunities of research trends of cytostatic drugs (and their derivatives) in the environment have been identified and critically discussed. This review provides an overview of risk assessment of pyrimidine antimetabolites and topoisomerase inhibitors, which is need of the hour considering their increasing consumption and state-of-the-art analytical detection. The main focus of the review is that a cocktail mixture of tamoxifen, 5-fluorouracil and other active metabolites of polar, water soluble antineoplastic agents may have the accumulation effect on the aquatic species. They can spread drug resistance via their interaction with some kinases.
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