4.7 Article

Polyester microplastic fibers induce mitochondrial damage, apoptosis and oxidative stress in Daphnia carinata, accompanied by changes in apoptotic and ferroptosis pathway

Journal

AQUATIC TOXICOLOGY
Volume 263, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.aquatox.2023.106690

Keywords

Microplastic fibers; odocera; Oxidative stress; Cellular death; Toxicology

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With the widespread use of plastic products, microplastic fibers have emerged as a new environmental contaminant, posing potential risks to planktonic organisms and aquatic ecosystems. This study investigated the toxicological effects of polyester microplastic fibers on a freshwater crustacean, revealing decreased survival and reproduction rates, as well as damage to mitochondria, increased apoptosis, oxidative stress and alterations in gene expression.
With the widespread utilization of plastic products, microplastics (MPs) have merged as a newfound environ-mental contaminant in the United States, and the bulk of these MPs in the environment manifest as fibrous structures. Concerns have also been voiced regarding the potential hazards posed by microplastic fibers (MFs). However, research examining the toxicity of MFs, particularly in relation to planktonic organisms, remains severely limited. Meanwhile, polyester fiber materials find extensive applications across diverse industries. As a result, this investigation delved into the toxicology of polyester microplastic fibers (PET-MFs) with a focus on their impact on Daphnia carinata (D. carinata), a freshwater crustacean. Newly hatched D. carinata were subjected to varying concentrations of PET-MFs (0, 50, and 500 MFs/mL) to scrutinize the accumulation of PET-MFs within these organisms and their resultant toxicity. The outcomes revealed that D. carinata was capable of ingesting PET-MFs, leading to diminished rates of survival and reproduction. These effects were accompanied by mito-chondrial impairment, heightened mitochondrial count, apoptosis, escalated generation of reactive oxygen species, augmented activity of antioxidant enzymes, and distinct patterns of gene expression. Interestingly, when comparing the group exposed to 50 MFs/mL with the one exposed to 500 MFs/mL, it was observed that the former triggered a more pronounced degree of mitochondrial damage, apoptosis, and oxidative stress. This phenomenon could be attributed to the fact that brief exposure to 500 MFs/mL resulted in greater mortality, eliminating individuals with lower adaptability. Those that survived managed to regulate elevated in vivo reactive oxygen species levels through an increase in glutathione S-transferase content, thereby establishing an adaptive mechanism. Low concentrations did not induce direct mortality, yet PET-MFs continued to inflict harm within the organism. RNA-seq analysis unveiled significant alterations in 279 and 55 genes in the 50 MFs/mL and 500 MFs/mL exposure groups, respectively. Functional enrichment analysis of the 50 MFs/mL group indicated involvement of the apoptosis pathway and ferroptosis pathway in the toxic effects exerted by PET-MFs on D. carinata. This study imparts valuable insights into the toxicological ramifications of PET-MFs on D. carinata, underscoring their potential risks within aquatic ecosystems.

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