Microcystin-LR in drinking water: An emerging role of mitochondrial-induced epigenetic modifications and possible mitigation strategies

Abstract

Algal blooms are a serious menace to freshwater bodies all over the world. These blooms typically comprise cyanobacterial outgrowths that produce a heptapeptide toxin, Microcystin-LR (MC-LR). Chronic MC-LR exposure impairs mitochondrial-nuclear crosstalk, ROS generation, activation of DNA damage repair pathways, apoptosis, and calcium homeostasis by interfering with PC/MAPK/RTK/PI3K signaling. The discovery of the toxin's biosynthesis pathways paved the way for the development of molecular techniques for the early detection of microcystin. Phosphatase inhibition-based bioassays, high-performance liquid chromatography, and enzyme-linked immunosorbent tests have recently been employed to identify MC-LR in aquatic ecosystems. Biosensors are an exciting alternative for effective on-site analysis and field-based characterization. Here, we present a synthesis of evidence supporting MC-LR as a mitotoxicant, examine various detection methods, and propose a novel theory for the relevance of MC-LR-induced breakdown of mitochondrial machinery and its myriad biological ramifications in human health and disease.