Circulating exosome level of indigenous fish may be a novel biomarker for the integrated ecotoxicity effect of water environment.

The deficiency of effective biomarker for the toxic effects of water pollutants greatly limits the application of biological monitoring. This study aimed to investigate the possibility of circulating exosomes of indigenous fish acting as biomarker for the ecotoxicity effect of water environment. The Helong Reservoir in Guangzhou, China, was chosen as the investigating field, of which the water quality belongs to Class V (2013) (GB 3838-2002, China). The clean drinking water source of the upper reaches of the Liuxihe Reservoir was selected as the control. Indigenous fishes including Oreochromis niloticus (Nile tilapia), Labeo rohita (Rohu), Carassius auratus (Crucian carp) were sampled during the period from July 2020 to April 2021. Circulating exosomes of fish samples were isolated by using ultracentrifugation, characterized with transmission electron microscopy (TEM) and quantified by using bicinchoninic acid (BCA) assay. Oxidative stress, DNA and chromosome damage in liver, kidney, brain, gill and blood of fish samples were measured. The results showed that there were significant differences in superoxide dismutase (SOD) activity, glutathione (GSH) and malondialdehyde (MDA) contents, DNA and chromosome damage in fish samples between the Helong Reservoir and the control. Interestingly, there were also significant differences in circulating exosome levels of fish samples between them. Our data suggested that circulating exosome level of indigenous fish may be a novel biomarker for the ecotoxicity effects of water environment.

Exosomal secretion may be a self-protective mechanism of its source cells under environmental stress: A study on human bronchial epithelial cells treated with hydroquinone.

Accumulating evidence reveals that exosome plays an important role in cell-to-cell communication in both physiological and pathological processes by transferring bioactive molecules. However, the role of exosomal secretion in the adaption of its source cells to the stimuli of environmental chemicals remains elusive. In this study, we revealed that the exposure of hydroquinone (HQ; the main bioactive metabolite of benzene) to human bronchial epithelial cells (16HBE) resulted in decreased ability of cell proliferation and migration, and simultaneously DNA damage and micronuclei formation. Interestingly, when exosomal secretion of HQ treated 16HBE cells was inhibited with the inhibitor GW4869, cellular proliferation and migration were further significantly reduced; concurrently, their DNA damage and micronuclei formation were both further significantly aggravated. Herein, we conclude that exosomal secretion of 16HBE cells may be an important self-protective function against the toxic effects induced by HQ.

Exosomal miR-221 derived from hydroquinone-transformed malignant human bronchial epithelial cells is involved in cell viability of recipient cells.

miR-221, an oncogenic microRNA, can promote cell proliferation and is highly expressed in various types of tumors. However, the role of exosomal miR-221 in benzene-caused carcinogenesis remains elusive. Our study was designed to investigate whether exosomes secreted by the hydroquinone (HQ; an active metabolite of benzene)-transformed malignant cells can transmit miR-221 to normal recipient cells and its possible effects on cell viability. Our investigation revealed that expression levels of miR-221 were significantly increased in HQ-transformed malignant cells relative to normal controls. Furthermore, exposure of control cells to exosomes that were derived from HQ-transformed malignant cells increased miR-221 levels and promoted their proliferation. Analyses of the biological potency of exosomes derived from HQ-transformed malignant cells in which miR-221 levels were decreased using an inhibitor, showed that both miR-221 levels and proliferation of recipient cells were decreased, but still were higher than those of normal 16HBE cells. Our study indicates that exosomal miR-221 derived from HQ-transformed malignant human bronchial epithelial cells is involved in the proliferation of recipient cells.

miR-222/GAS5 is involved in DNA damage and cytotoxic effects induced by temozolomide in T98G cell line.

Temozolomide (TMZ), a therapeutic DNA alkylator that can cause lethal DNA damage in cancer cells, is widely used for the standard chemotherapy against glioblastoma. However, long-term treatment with TMZ often causes drug resistance and poor prognosis, the mechanism of which remains largely unclear. This study aimed to investigate the possible role of miR-222/GAS5 axis on DNA damage and cytotoxic effects induced by TMZ in glioblastoma cells (T98G). Data suggest that the DNA comet tail length of T98G is positively correlated with the levels of miR-222 (R2  = 0.9808, P < 0.05), and negatively correlated with the levels of GAS5 (R2  = 0.8903, P < 0.05). The optical density value of T98G is negatively correlated with the levels of miR-222 (R2  = 0.7848, P < 0.05), and positively correlated with the levels of GAS5 (R2  = 0.6886, P < 0.05). Furthermore, comet tail length and optical density value are negatively and positively correlated with the levels of O-6-methylguanine-DNA methyltransferase, respectively (R2  = 0.8462, P < 0.05; R2  = 0.7018, P < 0.05). In conclusion, miR-222/GAS5 is involved in DNA damage and cytotoxic effects induced by TMZ, which means that miR-222/GAS5 may have great potential of being used as a biomarker for screening of chemotherapeutic alkylators.

Indigenous Fish-Based Assessment of Genotoxic Potentials of the Helong Reservoir in Guangzhou, China.

The present study was conducted to assess the genotoxic potential of water from the Helong Reservoir, which was designated as a strategic drinking water source by the Guangdong Provincial Government of China in October 2016. Four kinds of common indigenous fish samples (Labeo rohita, Cirrhinus molitorella, red tilapia, and Oreochromis niloticus) were collected at 6 sampling sites during the period from July to November 2020. Fish from the clean drinking water source of the upper reaches of the Liuxihe Reservoir in Guangzhou were collected as the control. Both the alkaline single cell gel electrophoresis assay and the micronucleus test were used to detect DNA damage and the micronucleus rate in erythrocytes of fish samples, respectively. The results indicated that there was a significant increase in comet tail length, Olive tail moment, and micronucleus rates of all fish samples compared with those of the control (p < 0.05). The order of sensitivity to DNA damage and micronucleus formation was Labeo rohita > Cirrhinus molitorella > red tilapia > Oreochromis niloticus. The results of the 2 kinds of experiments were in perfect agreement with each other. We conclude that there are obvious genotoxic effects from the water in the Helong Reservoir. As a strategic drinking water source, the safety of the Reservoir water quality should be considered. The local government should put the restoration of the Helong Reservoir water quality on the agenda as soon as possible. Environ Toxicol Chem 2021;40:1919-1927. © 2021 SETAC.

EDTA-functionalized magnetic chitosan oligosaccharide and carboxymethyl cellulose nanocomposite: Synthesis, characterization, and Pb(II) adsorption performance.

A novel ethylenediaminetetraacetic acid (EDTA)-functionalized magnetic chitosan oligosaccharide and carboxymethyl cellulose (Fe3O4@CMCCOS-EDTA) nanocomposite adsorbent was successfully fabricated for Pb(II) adsorption. The adsorbent was characterized by Fourier transform infrared, and X-ray photoelectron spectroscopy was used to confirm successful EDTA modification and Pb(II) adsorption. Scanning electron microscopy, transmission electron microscopy, vibrating sample magnetometer, and thermogravimetric analysis were used to study the morphology and properties of magnetic particles. EDTA modification considerably improved the capacity of the adsorbent. The batch adsorption experiment results indicated that the pseudo-second-order (PSO) model and the Langmuir isotherm model reliably described the adsorption behavior. The maximum adsorption capacity (qm) for monolayer chemical adsorption was calculated to be 432.34 mg/g at the pH of 5 and temperature of 308 K. Notably, Fe3O4@CMCCOS-EDTA exhibited a high Pb(II) removal rate of ~100% using an initial metal ion solution of 100 mg/L and 200 mg/L.

Adsorption of Pb(II) from aqueous solution by polyacrylic acid grafted magnetic chitosan nanocomposite.

A creative combination of chitosan with polyacrylic acid (PAA) improves the acidity resistance of chitosan and increases its potential in the field of adsorption. In order to facilitate recovery, magnetic nanoparticles were incorporated in CS-PAA to obtain a magnetic-CS-PAA (MCS-PAA) nanocomposite. The physical and chemical characteristics of the composite adsorbent MCS-PAA were determined by SEM, TEM, FTIR, EDX, XRD, and XPS. This environmental-friendly, magnetic, composite adsorbent showed significantly better adsorption performance than those of the individual adsorbents alone. The maximal adsorption capacity was 204.89 mg/g according to the Langmuir isotherm model, when the concentration of Pb(II) was 100 mg/L at the equilibrium time of 70 min. The main adsorption mechanism was the complexation between the carboxyl, amino, and hydroxyl groups in MCS-PAA and Pb(II). Further, introduction of PAA also improved the acid resistance of CS. The new adsorbent MCS-PAA is thus expected to facilitate a wider range of applications for chitosan in the adsorption of Pb(II).

Exosomes derived from normal human bronchial epithelial cells down-regulate proliferation and migration of hydroquinone-transformed malignant recipient cells via up-regulating PTEN expression.

The gene encoding the tumor suppressor, phosphatase and tensin homolog (PTEN), located on chromosome 10, is frequently expressed at low levels in various tumors, resulting in the stimulation of cell proliferation and migration. However, the role of exosomal PTEN in cell-cell communication during the progress of benzene-induced carcinogenesis remains unclear. The goal of this study was to explore whether exosomes derived from normal human bronchial epithelial cells (16HBE) could transmit PTEN to hydroquinone-transformed malignant recipient cells (16HBE-t) and its possible effects on cell proliferation and migration. Consistent with PTEN expression being down-regulated in transformed cells, we found that its expression was significantly decreased in 16HBE-t relative to 16HBE cells and that purified exosomes secreted by 16HBE, up-regulated PTEN levels in recipient 16HBE-t cells. Thus, down-regulating their proliferation and migration. Further, when exosomes derived from 16HBE cells that had been treated with the PTEN inhibitor SF1670, were incubated with recipient 16HBE-t cells, they exhibited decreased PTEN levels, with a corresponding increase in their proliferation and migration. In conclusion, our study demonstrates that exosomes derived from 16HBE cells can down-regulate proliferation and migration of recipient 16HBE-t cells via transferring PTEN.