MCF-7 cell - derived exosomes were involved in protecting source cells from the damage caused by tributyltin chloride via transport function.

Tributyltin chloride (TBTC) is a ubiquitous environmental pollutant with various adverse effects on human health. Exosomes are cell - derived signaling and substance transport vesicles. This investigation aimed to explore whether exosomes could impact the toxic effects caused by TBTC via their transport function. Cytotoxicity, DNA and chromosome damage caused by TBTC on MCF-7 cells were analyzed with CCK-8, flow cytometry, comet assay and micronucleus tests, respectively. Exosomal characterization and quantitative analysis were performed with ultracentrifugation, transmission electron microscope (TEM) and bicinchoninic acid (BCA) methods. TBTC content in exosomes was detected with Liquid Chromatography-Mass Spectrometry (LC-MS). The impacts of exosomal secretion on the toxic effects of TBTC were analyzed. Our data indicated that TBTC caused significant cytotoxicity, DNA and chromosome damage effects on MCF-7 cells, and a significantly increased exosomal secretion. Importantly, TBTC could be transported out of MCF-7 cells by exosomes. Further, when exosomal secretion was blocked with GW4869, the toxic effects of TBTC were significantly exacerbated. We concluded that TBTC promoted exosomal secretion, which in turn transported TBTC out of the source cells to alleviate its toxic effects. This investigation provided a novel insight into the role and mechanism of exosomal release under TBTC stress.

mTORC1 - TFEB pathway was involved in sodium arsenite induced lysosomal alteration, oxidative stress and genetic damage in BEAS-2B cells.

The mechanistic target of rapamycin (RAPA) complex 1 (mTORC1) - transcription factor EB (TFEB) pathway plays a crucial role in response to nutritional status, energy and environmental stress for maintaining cellular homeostasis. But there is few reports on its role in the toxic effects of arsenic exposure and the related mechanisms. Here, we show that the exposure of bronchial epithelial cells (BEAS-2B) to sodium arsenite promoted the activation of mTORC1 (p-mTORC1) and the inactivation of TFEB (p-TFEB), the number and activity of lysosomes decreased, the content of reduced glutathione (GSH) and superoxide dismutase (SOD) decreased, the content of malondialdehyde (MDA) increased, the DNA and chromosome damage elevated. Further, when mTORC1 was inhibited with RAPA, p-mTORC1 and p-TFEB down-regulated, GSH and SOD increased, MDA decreased, the DNA and chromosome damage reduced significantly, as compared with the control group. Our data revealed for the first time that mTORC1 - TFEB pathway was involved in sodium arsenite induced lysosomal alteration, oxidative stress and genetic damage in BEAS-2B cells, and it may be a potential intervention target for the toxic effects of arsenic.

Image detection model construction of Apolygus lucorum and Empoasca spp. based on improved YOLOv5.

BACKGROUND: The polyphagous mirid bug Apolygus lucorum (Meyer-Dür) and the green leafhopper Empoasca spp. Walsh are small pests that are widely distributed and important pests of many economically important crops, especially kiwis. Conventional monitoring methods are expensive, laborious and error-prone. Currently, deep learning methods are ineffective at recognizing them. This study proposes a new deep-learning-based YOLOv5s_HSSE model to automatically detect and count them on sticky card traps. RESULTS: Based on a database of 1502 images, all images were collected from kiwi orchards at multiple locations and times. We trained the YOLOv5s model to detect and count them and then changed the activation function to Hard swish in YOLOv5s, introduced the SIoU Loss function, and added the squeeze-and-excitation attention mechanism to form a new YOLOv5s_HSSE model. Mean average precision of this model in the test dataset was 95.9%, the recall rate was 93.9% and the frames per second was 155, which are higher than those of other single-stage deep-learning models, such as SSD, YOLOv3 and YOLOv4. CONCLUSION: The proposed YOLOv5s_HSSE model can be used to identify and count A. lucorum and Empoasca spp., and it is a new, efficient and accurate monitoring method. Pest detection will benefit from the broader applications of deep learning. © 2024 Society of Chemical Industry.

Lysosome-related exosome secretion mediated by miR-26b / Rab31 pathway was associated with the proliferation and migration of MCF-7 cells treated with BPA.

Bisphenol A (BPA), one of the typical environmental endocrine disruptors (EEDs), can promote the proliferation and migration of cancer cells, but the mechanism of which remains largely unclear. Exosome secretion plays an important role in the stress response of cells to environmental stimuli. This study was designed to explore whether exosome secretion was involved in the toxic effect of BPA on the proliferation and migration of MCF-7 cells, and the related mechanism. Our data shows that the IC50 value of MCF-7 exposure to BPA was about 65.82 µM. The exposure of MCF-7 to 10 µM BPA resulted in a decreased miR-26b expression and the activation of miR-26b/Rab-31 pathway, consequently, the number and activity of lysosomes decreased, the secretion of exosomes increased, cell proliferation and migration were enhanced obviously. Interestingly, miR-26b mimic up-regulated the number and activity of lysosomes via miR-26b/miR-31 pathway, exosome secretion was down-regulated, cell proliferation and migration decreased. Further, when GW4869 was used to directly inhibit the exosome secretion of MCF-7 treated with BPA, their proliferation and migration were down-regulated. Herein, we concluded that the stimulating effect of BPA on the proliferation and migration of MCF-7 cells was associated with the lysosome - related exosome secretion via miR-26b / Rab31 pathway.

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.

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.

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.

Temperature-Mediated Effects of Host Alternation on the Adaptation of Myzus persicae (Hemiptera: Aphididae).

Local adaptation, an important phenomenon in ecological speciation, occurs in Myzus persicae (Sulzer), with the tobacco-adapted line proposed as a subspecies. Recent studies showed that temperature could alter the selection strength and direction in host-herbivore interactions. To understand the formation of host-adapted speciation and the effects of temperature on host adaptation, the parthenogenetic progeny of an M. persicae egg were conditioned on two hosts for >10 generations. Then, their life table parameters were studied after reciprocal transfer under a temperature gradient. The results showed that aphids habituated on tobacco (Nicotiana tabacum L.) and rape (Brassica napus L.) had different optimal temperatures, including different upper thresholds of development and reproduction on original and alternative hosts. After habituation for >10 generations, local adaptation of aphids on the host of origin was formed, which was observed as the better performance of the native aphids compared with the foreign ones. The M. persicae that habituated on rape appeared more generalized to the host plants than the aphids that habituated on tobacco. The adaptation patterns of green peach aphids on two hosts varied differentially according to temperature, which verified the temperature-mediated effects of host selection on herbivores, implying the presence of a demographic basis of aphid seasonal migration.

The effects of enhanced ultraviolet-B radiation on the biology of green and brown morphs of Sitobion avenae (Hemiptera: Aphididae).

The effects of enhanced UV-B radiation on the biology of green and brown morphs of Sitobion avenae (F.) (Hemiptera: Aphididae) were tested under laboratory conditions. The two S. avenae morphs were exposed directly to different doses (0, 216, 432, and 864 kJ/m(2)) of artificial UV-B. Under low doses of UV-B (216 kJ/m(2)), the nymphal development period was significantly shorter, whereas mean relative growth, total fecundity, and gross reproductive rate were significantly higher for both aphid morphs compared with those morphs under control treatments (0 kJ/m(2)). Under high doses of UV-B (432 kJ/m(2) and/or 864 kJ/m(2)), the nymphal development period was significantly longer, whereas the reproductive period, postreproductive period, difference in weight, mean relative growth, and life table parameters were significantly reduced for both aphid morphs. Moreover, the nymphal development period was significantly shorter and the differences in weight, mean relative growth, total fecundity, and life table parameters were significantly higher for the brown morph under high doses of UV-B compared with the green morph. The results showed that enhanced UV-B affects the performance of the green and brown S. avenae morphs from positively to negatively. The brown morph exhibited stronger adaptability than the green morph at high doses of UV-B.

Life table evaluation of survival and reproduction of the aphid, Sitobion avenae, exposed to cadmium.

The effects of cadmium (Cd) on the development, fecundity, and reproduction of the grain aphid, Sitobion avenae Fabricius (Hemiptera: Aphididae) were estimated by constructing a life table of S. avenae exposed to Cd. The concentrations of Cd in the soil were as follows: 0, 10, 20, 40, 80, and 160 mg/kg. The correlation analysis of the Cd concentration in soil and wheat revealed that the amount in the wheat increased with the increase of Cd concentrations in soil. The results indicated that, the latter part of the reproduction period was significantly affected by Cd, according to the curve of the total survival rate (l(x)). The net reproductive rate (R(0)), innate capacity of increase (r), and finite rate of increase (λ) of S. avenae all decreased under the stress of Cd, and were lowest at a Cd concentration of 20 mg/kg. Cd also negatively affected fecundity and m(x) (the number of offspring produced by an individual female). At 20 mg/kg, the decline of them was most obvious. In conclusion, survival and reproduction of S. avenae were inhibited under the treatment of the heavy metal Cd. Sitobion avenae was more sensitive to Cd at concentration of 20 mg/kg compared to the other concentrations. This concentration can be used to examine the mechanisms behind population genetics and biological mutation of S. avenae when exposed to heavy metal.

[Effects of UV-radiation on biological characteristics of different body-color biotypes of Sitobion avenae (Fab.)].

UV-radiation exerts strong selection stress on the evolution of aphid populations, and thus, leads to their genetic differentiation. However, the effects of UV-radiation on different body-color biotypes of aphids are still ambiguous. In this study, new-born nymphae of red and green biotypes of Sitobion avenae were placed on two wheat varieties (Xiaoyan-22 and Astron), bred in an artificial bioclimatic chamber under strict controlled conditions (at 15 degrees C, 20 degrees C, and 25 degrees C, and treated with 30 W lamp of UV-B for 30 min per day for 5 days), and their development duration, mass, and mean relative growth rate were measured. The results showed that at lower temperature, UV-radiation delayed the growth of green biotype aphid on Xiaoyan-22 and Astron significantly; while at higher temperature, UV-radiation significantly delayed the growth of red biotype aphid on Xiaoyan-22, but had lesser effects on the growth of the two biotypes on Astron, illustrating that different biotypes of aphids had different responses to UV-radiation, and the responses were correlated to temperature and wheat varieties.