Exposure to Polypropylene Microplastics via Oral Ingestion Induces Colonic Apoptosis and Intestinal Barrier Damage through Oxidative Stress and Inflammation in Mice

Abstract

Extensive environmental pollution by microplastics has increased the risk of human exposure to plastics. However, the biosafety of polypropylene microplastics (PP-MPs), especially of PP particles < 10 μm, in mammals has not been studied. Thus, here, we explored the mechanism of action and effect of exposure to small and large PP-MPs, via oral ingestion, on the mouse intestinal tract. Male C57BL/6 mice were administered PP suspensions (8 and 70 μm; 0.1, 1.0, and 10 mg/mL) for 28 days. PP-MP treatment resulted in inflammatory pathological damage, ultrastructural changes in intestinal epithelial cells, imbalance of the redox system, and inflammatory reactions in the colon. Additionally, we observed damage to the tight junctions of the colon and decreased intestinal mucus secretion and ion transporter expression. Further, the apoptotic rate of colonic cells significantly increased after PP-MP treatment. The expression of pro-inflammatory and pro-apoptosis proteins significantly increased in colon tissue, while the expression of anti-inflammatory and anti-apoptosis proteins significantly decreased. In summary, this study demonstrates that PP-MPs induce colonic apoptosis and intestinal barrier damage through oxidative stress and activation of the TLR4/NF-κB inflammatory signal pathway in mice, which provides new insights into the toxicity of MPs in mammals.

Elucidating the effects of naturally weathered aged-polypropylene microplastics and newly procured polypropylene microplastics on raw 264.7 macrophages

“…Another study offered preliminary data that oral consumption of PPMPs causes a redox system imbalance as colonic epithelial cells from mice indicated mitochondrial damage after being subjected to PPMPs with sizes of 8 μm and 70 μm and concentrations of 1 and 10 mg mL −1 , and minor abnormalities in mitochondrial structures, including vacuolation, loose ridge arrangement decreased matrix and partial swelling, were observed. 52 Meanwhile, another study consisting of a novel 3D in vitro intestinal model showed that MPs at concentrations of 823.5–1380 μg cm −2 of size 50–500 μm did not show any significant cytotoxicity as well as no changes in barrier integrity. 53 Another study, revealed that MP phagocytosis decreases murine macrophage mitochondrial respiration.…”

“…Another study provided fresh insight into the hazardous effects of MPs on mammals by showing that PPMPs (8 and 70 μm) can harm the intestinal barrier and cause colonic apoptosis in mice by oxidative stress and activation of the TLR4/NF-B inflammatory signal pathway. 110 Reactive oxygen species (ROS) and antioxidant enzymes like glutathione- S -transferase (GST), glutathione reductase (GR) and glutathione peroxidase (GPx) were induced in the monogonont rotifer ( Brachiounus koreanus ) in response to microplastics. 111 In our study, NP-PPMPs triggered higher apoptosis than aged-PPMPs.…”

Influence of polyethylene terephthalate (PET) microplastic on selected active substances in the intramural neurons of the porcine duodenum

“…Mucus present in the intestines has a protective function and prevents the adhesion of microorganisms [ 126 ]. Mice exposed to oral polypropylene showed a decrease in mucus production and the destruction of the intestinal mucosal barrier in response to oxidative damage and altered inflammatory cytokine levels [ 127 ]. It can be assumed that MP-PET initially caused the loss of microvilli, to which the body responded with increased mucus secretion as a defense mechanism.…”

Influence of Microplastics on Morphological Manifestations of Experimental Acute Colitis

“…Dysbiosis of the intestinal microflora was revealed in mice treated with MPs [ 21 , 22 , 23 , 24 , 25 ]. According to a number of authors, exposure to MPs causes mild or moderate inflammation in the colon, characterized by weak inflammatory infiltration of the mucosa, the activation of pro-inflammatory signaling pathways, and the increased expression of pro-inflammatory cytokines [ 17 , 23 , 24 , 26 , 27 , 28 , 29 , 30 ]. Violations of antioxidant defense and the development of oxidative stress were revealed [ 28 , 29 , 30 , 31 ].…”