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Objective To evaluate the immunotoxicity and effects of noise and/or low‐concentration carbon monoxide (CO) exposure on immune organs and immune functions in rats. Methods Male Wistar rats exposed to 98 dB(A) white noise and/or 100 ppm CO 4 h/d for 30 d were used to determine the pathological changes in the thymus and spleen, and variations in leukocyte counts, inflammatory factors, and immunoglobulin (Ig) concentrations. Results The boundaries of the cortex and medulla of the thymus were unclear following noise and combined exposure. The pathological changes in spleen after CO and combined exposure included blurred boundaries of red‐pulp and white‐pulp, disappearance of normal splenic nodules and neutrophil infiltration. After exposure to noise and in combination, leukocyte and lymphocyte counts decreased significantly. After exposure to low‐concentration CO and in combination, serum IgM and IgG levels decreased significantly, but the levels of tumor necrosis factor‐α and interferon‐γ levels increased significantly. Eosinophils and IgA levels decreased significantly following exposure to noise and/or low concentration of CO, while the level of interleukin‐1 increased significantly. Monocytes increased significantly only under noise or CO exposure, but not under combined exposure. Conclusions Noise and/or low‐concentration CO exposure may suppress innate and adaptive immune functions and induce inflammatory responses. Noise exposure mainly affected the innate immune function of rats, whereas low‐concentration CO exposure mainly affected adaptive immune functions. Combined exposure presented higher immunotoxicity than noise or CO alone, suggesting that exposure to noise and low‐concentration CO in the living and working environments can affect the immune system.

To clarify the cardiotoxicity induced by acute exposure to different concentrations of ozone in both gender rats and explore the underlying mechanisms.A total of 240 rats were randomly sorted into 6 groups with equal numbers of male and female rats in each group. The rats were subjected to ozone inhalation at concentrations of 0, 0.12, 0.5, 1.0, 2.0 and 4.0 ppm, respectively, for 6 h. After ozone exposure, function indicators, myocardial injury indexes and risk factors of cardiovascular disease in blood were assayed.High ozone exposure resulted in sustained ventricular tachycardia in male and female rats. Myocardial apoptosis in male rats started from 1.0 ppm ozone, and that in female rats started from 2.0 ppm ozone (p 0.05). Caspase-9 increased significantly from 0.12 ppm ozone (p 0.01) in both gender rats, while caspase-3 was initially activated at 0.5 ppm ozone. From 1.0 ppm ozone, mitochondrial cristae and myofilaments dissolved. The ratio of Bcl-2/Bax decreased significantly from 0.12 ppm and MRCC-IV decreased significantly from 2.0 ppm by ozone.Acute ozone exposure can cause paroxysmal ventricular tachycardia in rats. Moreover, the changes of inflammatory factors in the heart tissues of female and male rats after ozone exposure were greater than those of oxidative stress. This study reported for the first time that 6 h ozone exposure does not cause acute cardiomyocyte necrosis, but promotes cardiomyocyte apoptosis in a mitochondrial-dependent manner. Ozone could regulate caspases-3 dependent cardiomyocyte apoptosis by affecting the balance between caspase-9 and XIAP.

Thiazole-Zn is a systemic fungicide synthesized and developed in China that has been used for the prevention and treatment of bacterial and fungal diseases on fruits and vegetables. Thiazole-Zn is a new thyroid disruptor chemical. The purpose of this study was to clarify the thyroid-disrupting property of thiazole-Zn and the mechanism responsible for thyroid hormone (TH) biosynthesis inhibition in male rats induced by thiazole-Zn. First, the effects of different thiazole-Zn doses and exposure times on the thyroid weights, thyroid morphology and serum hormone levels of rats were investigated. The results showed that thiazole-Zn increased thyroid weights and serum thyroid-stimulating hormone (TSH) levels and induced thyroid cell hypertrophy and hyperplasia in a dose-related and time-related manner. Furthermore, measurement of thyroid radioiodine uptake in vivo in rats confirmed that thiazole-Zn inhibited active iodide uptake into the thyroid, which reduced circulating levels of serum T3 and T4. Decreases in circulating THs resulted in a compensatory increase in serum TSH levels through a negative feedback system. Subsequently, sustained excessive stimulation of the thyroid gland by TSH led to thyroid follicular cell hypertrophy and hyperplasia. In addition, thiazole-Zn increased sodium/iodide symporter (NIS) expression in the rat thyroid, and the increased NIS expression promoted and restored iodide uptake into the thyroids of rats. The risk of iodine intake inhibition by thiazole-Zn to humans, especially susceptible individuals, such as children and pregnant women, warrants additional attention.

Objective Ozone has become a major air pollutant in recent years, which leading to a variety of lung diseases. This study aimed to explore the mechanisms of pyroptosis and related signaling pathways in ozone-induced lung injury. Methods We exposed 120 Wistar rats to ozone, 20 in each group (half male and half female). Ozone exposure concentrations were 0, 0.12, 0.5, 1.0, 2.0 and 4.0 ppm for 6 h. At the same time, we isolated and cultured type I alveolar epithelial cells, then intervened with high mobility group box 1 protein (HMGB1), hyaluronic acid (HA) and Toll-like receptors 2/4 (TLR2/4) inhibitor. In animal experiments, histopathological experiments, TUNEL, ELISA and biochemical indicators were performed. RT-qPCR and western blot experiments assay were used to detect the expression changes of key factors in relevant signal pathways in vivo and in vitro. Results After acute ozone exposure, the levels of lung cell injury indicators in bronchoalveolar lavage fluid (BALF), as well as the levels of inflammatory factors in BALF, blood, and lung tissue were significantly increased. Male rats were more sensitive to ozone exposure. Low-concentration ozone exposure caused mild interstitial inflammation in rat lung tissue. Severe inflammation and pulmonary edema appeared with increases in concentration. ELISA results in BALF showed that HMGB1 and HA expressions increased gradually with the increase of ozone exposure concentration. RT-qPCR and Western blot showed that when ozone concentrations increased above 0.5 ppm, the expression of nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3 (NLRP3), cleaved caspase-1, and N-gasdermin D (N-GSDMD) in the lung tissue increased significantly, suggesting that ozone exposure induces pyroptosis. At the same time, it was found that ozone exposure activated the nuclear factor kappa B (NF-κB) signal pathway, and increased the mRNA expressions of Toll-like receptors TLR2/4. The results of cell experiments showed that after the addition of HMGB1 and HA, the expression of NF-κB and pyroptosis related indexes increased in type I alveolar epithelial cells, while the corresponding expression decreased after the addition of TLR2/4 inhibitors. Conclusion Ozone exposure causes lung injury in a dose- and gender-dependent manner, and is more severe in males. When injured, the levels of HMGB1 and HA in BALF increased, which interact with TLR 2/4 to activate the downstream NF-κB signaling pathway. Further activating the NLRP3 inflammasome complex and regulating the ozone-induced pyroptosis.

Chronic noise exposure has been implicated in increased risk of diabetes. However, there is limited experimental evidence of the mechanisms linking chronic noise stress and glucose metabolism. We addressed this in the present study by examining glucose metabolism, immune response, and changes in gut microbiota/host inflammatory homeostasis in rats exposed to noise for 30 consecutive days. Chronic noise exposure increased blood glucose and corticosterone levels for at least 14 days after cessation of noise. Stressed rats also exhibited elevated levels of glycogen and triglyceride in the liver and impaired hepatic insulin production via insulin-induced insulin receptor/insulin receptor substrate 1/glycogen synthase kinase 3β signalling, which persisted for 3–14 days after cessation of noise exposure. Chronic noise altered the percentage of Proteobacteria and Actinobacteria in the gut, increasing Roseburia but decreasing Faecalibacterium levels in the cecum relative to controls. Immunoglobulin A, interleukin 1β, and tumor necrosis factor α levels were also elevated in the intestine of these animals, corresponding to noise-induced abnormalities in glucose regulation and insulin sensitivity. These results suggest that lifelong environmental noise exposure could have cumulative effects on diabetes onset and development resulting from alterations in gut microbiota composition and intestinal inflammation.

The expanded application of carbon nanotubes and increased annual production has recently sparked public interest concerning associated and potentially adverse exposure effects. As very little is known with regard to the toxicology and underlying mechanism of the phenomena termed "single-walled carbon nanotube (SWCNT) exposure", we conducted an in depth investigation of potential SWCNT effects on cell adhesion molecule gene expression within rat aortic endothelial cells (RAECs). RAEC exposure to SWCNT induced neutrophil adhesion to the endothelial monolayer via increased ICAM-1 and VCAM-1 expression. Due to NF-kappaB's fundamental involvement in the transcriptional regulation of cell adhesion molecules, we studied NF-kappaB/P65 activation in SWCNT treated RAECs, as well as GSH and LDH as determinants of oxidative stress, a condition that influences NF-kappaB activation. Resultant data indicates SWCNT exposure induces oxidative stress, thereby altering ICAM-1 and VCAM-1 expression. SWCNT induced nuclear NF-kB/P65 translocation can be inhibited by N-acetylcysteine, indicating elevated ICAM-1 and VCAM-1 expression is mediated by oxidative stress in RAECs, and may play important inflammatory roles in SWCNT-induced vascular endothelium damage.