Polylactic Acid-Based Microplastic Particles Induced Oxidative Damage in Brain and Gills of Goldfish Carassius auratus

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Abstract

The effect of 96 h exposure of the goldfish Carassius auratus to two different types of bioplastic particles, originating from commercial shopping bag (Bag, ~5 mm) and polylactic acid-based (PLA) cup (Cup, ≤5 mm), and petroleum-based polyamide particles (PA, 0–180 µm) was studied. All particles were studied as virgin and after simulated UV-degradation (at concentration 30 mg L−1). The experiments were conducted according to OECD 203 test guidelines. The toxicity endpoint evaluated in fish brain and gills was lipid peroxidation (LPO) quantified as nmol thiobarbituric acid reactive substances (TBARs) mg−1 protein. The results indicated that indicatively compostable PLA bioplastic Cup induced significant LPO in the brain and/or gills of the goldfish, in contrast to the particles from Bag and PA (in the brain, Cup > Bag > PA; in the gills, Cup > Bag). The UV-degradation of the particles of all studied types had no significant effect on the LPO level compared to virgin particles. While the increase of LPO in fish gills and brain upon exposure to PLA-plastic particles can be transitory in the long-term perspective, our results point to the necessity of a thorough investigation of the hazard of bioplastics at different state of environmental degradation/weathering.

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Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

Antonio Ayala, Mario F Muñoz, Sandro Argüelles (2014)

Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

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At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, however, nitric oxide (NO), superoxide anion, and related reactive oxygen species (ROS) play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and reestablish "redox homeostasis." Higher organisms, however, have evolved the use of NO and ROS also as signaling molecules for other physiological functions. These include regulation of vascular tone, monitoring of oxygen tension in the control of ventilation and erythropoietin production, and signal transduction from membrane receptors in various physiological processes. NO and ROS are typically generated in these cases by tightly regulated enzymes such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. In a given signaling protein, oxidative attack induces either a loss of function, a gain of function, or a switch to a different function. Excessive amounts of ROS may arise either from excessive stimulation of NAD(P)H oxidases or from less well-regulated sources such as the mitochondrial electron-transport chain. In mitochondria, ROS are generated as undesirable side products of the oxidative energy metabolism. An excessive and/or sustained increase in ROS production has been implicated in the pathogenesis of cancer, diabetes mellitus, atherosclerosis, neurodegenerative diseases, rheumatoid arthritis, ischemia/reperfusion injury, obstructive sleep apnea, and other diseases. In addition, free radicals have been implicated in the mechanism of senescence. That the process of aging may result, at least in part, from radical-mediated oxidative damage was proposed more than 40 years ago by Harman (J Gerontol 11: 298-300, 1956). There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.