Mitochondrial dysfunctions elicited by solid waste leachates provide insights into mechanisms of leachates induced cell death and pathophysiological disorders
2022
Alimba, Chibuisi Gideon | Sivanesan, Saravanadevi | Krishnamurthi, Kannan
Emissions (mainly leachates and landfill gases) from solid waste facilities are laden with mixtures of dangerous xenobiotics implicated with significant increase in various pathophysiological disorders including cancer, and eventual mortality of exposed wildlife and humans. However, the molecular mechanisms of solid waste leachates induce pathophysiological disorders and cell death are still largely unknown. Although, evolving evidence implicated generation of reactive oxygen species and oxidative stress as the possible mechanism. Recent scientific reports are linking reactive oxygen species and mitochondrial dysfunctions as the player mechanism in pathophysiological disorder and apoptosis induced by xenobiotics in solid waste leachates. This systematic review presents an explicit discussion of recent scientific findings on the structural and functional alterations in mitochondria induced by solid waste leachates as the molecular mechanisms plausibly responsible for the pathophysiological disorders, cancer and cell death reported in landfill toxicology and epidemiological studies. This review aims to increase scientific understanding on solid waste leachate induced mitochondria dysfunctions as the key player in molecular mechanisms of solid waste induced toxicity. The findings in this review were mainly from using primary cells, cell lines, Drosophila and fish. Whether the findings will similarly be observed in mammalian test systems in vivo and particularly in exposed humans, remained to be investigated. Improvement in technological advancements, enforcement of legislation and regulations, and creation of sophisticated health surveillance against exposure to solid waste leachates, will expectedly mitigate human exposure to solid waste emissions and contamination of the environment.
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