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Mitochondria and endoplasmic reticulum (ER) are essential organelles playing pivotal roles in the regulation of cellular metabolism, energy production, and protein synthesis. In addition, these organelles are important targets susceptible to external stimuli, such as environmental pollutants. Exposure to environmental pollutants can cause the mitochondrial damage, endoplasmic reticulum stress (ERS), and oxidative stress, leading to cellular dysfunction and death. Therefore, understanding the toxic effects and molecular mechanisms of environmental pollution underlying these processes is crucial for developing effective strategies to mitigate the adverse effects of environmental pollutants on human health. In the present study, we summarized and reviewed the toxic effects and molecular mechanisms of mitochondrial damage, ERS, and oxidative stress caused by exposure to environmental pollutants as well as interactions inducing the cell apoptosis and the roles in exposure to environmental pollutants.

ABSTRACTNanoplastics, an emerging contaminant, pose risks to fetal neural development, transferring from mother to offspring via placenta and breast milk. Assessing these risks, hippocampal CA3 samples from nanopolystyrene-exposed rat offspring were proteomically analyzed. Findings revealed reduced expression of neural developmental proteins (KIF21A, STMN2, DMTN, DLG1) and increased inhibitory proteins (PZP, α-2M, FN1, SERPINA1, ALOX15) in the hippocampus. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis highlighted ferroptosis enrichment, validated by significantly expressed ALOX15 and TF proteins. These alterations suggest nanopolystyrene’s potential contribution to cognitive deficits and neurodevelopmental disorders, emphasizing its hazardous impact on neural development. This study provides novel insights into nanopolystyrene’s risks.

Background: Exposure to heavy metals during pregnancy is an important risk factor for adverse birth outcomes. We aimed to investigate the current heavy metal exposure levels in cord blood from healthy pregnant women residing in the Huaihe River Basin, China, and examined the association between heavy metal levels and dietary habits and lifestyle factors. In this study, we measured the exposure levels of five heavy metals in the umbilical cord blood from 350 healthy pregnant women and administered 350 self-reported questionnaires regarding the general characteristics and dietary habits of those women. Methods: This study was undertaken in Shenqiu county, Henan province, which is in the area of the Huai River Basin, in a cohort of pregnant women and newborn babies in 2013–2014. We recruited a sample of 1000 pregnant women among those receiving prenatal examination, measured the real individual newborn exposure to heavy metals in serum by ICP-MS, collected information regarding the pregnant women with a questionnaire survey and obtained data on environmental quality from environmental protection agencies and the available literature. We estimated the daily individual exposure to heavy metals of all the 1000 participants throughout the pregnancy and recorded their birth outcomes after delivery. Then we analyzed the association between birth outcome and individual exposure to heavy metals. Results: 54 newborn children had birth defects. The geometric means of cord blood levels of As, Cd, Cr, Pb and Hg were measured at 0.92 ± 1.01 ng mL−1, 0.11 ± 0.17 ng mL−1, 4.57 ± 5.02 ng mL−1, 3.37 ± 3.81 ng mL−1and 0.89 ± 1.69 ng mL−1for subjects (n= 54) who gave birth to infants with birth defects and 0.43 ± 0.88 ng mL−1, 0.52 ± 3.86 ng mL−1, 1.94 ± 2.92 ng mL−1, 4.38 ± 4.96 ng mL−1and 0.43 ± 0.91 ng mL−1for subjects (n= 296) with healthy infants, respectively. The contents of all five heavy metals in the whole blood of both of these two groups were higher than the reference values of the Chinese general population (P< 0.001). Conclusions: The occurrence of birth defects was 15.4% in this cohort, and was correlated to exposure of parents to environments containing heavy metal contaminants in Shenqiu county in the Huai River Basin. The heavy metal exposure situation of the investigated population had serious effects in terms of reproductive defects in children. The specific link between newborn defects and environmental heavy metal contaminants suggested that contamination in pregnant women persisted over time, and that the exposure may have a long term effect.

Previous studies demonstrated that tris(1,3-dichloro-2-propyl)phosphate (TDCIPP) caused adverse effects on thyroid hormone (TH) imbalance in aquatic and avian organisms. This study focused on the effects of TDCIPP on thyroid function and hormone homeostasis in mammals. Pubertal female Sprague-Dawley rats were orally administered 50, 100, or 250 mg per kg per d of TDCIPP from postnatal day (PND) 22 to PND42 for 21 days. The serum triiodothyronine (T3) levels increased significantly at 250 mg per kg per d of TDCIPP. There were no significant differences in the body weight, serum thyroxine (T4) and free thyroxine (FT4) levels between the control and TDCIPP treated groups. There were significant dose-dependent increases in the mRNA and protein expression levels of genes related to drug metabolism (cytochrome-p450-3A1, CYP3A1) and TH clearance (udp-glucuronosyltransferase-1A6, UGT1A6) in the liver. Treatment with TDCIPP increased hepatic type 1 deiodinase (DIO1) mRNA at 250 mg per kg per d but down-regulated hepatic TH receptor beta (TRβ) mRNA expression. In addition, TDCIPP exposure induced slight thyroid follicular hyperplasia, and several genes involved in TH biosynthesis (NIS, TPO, Tg) were altered at 100 and 250 mg per kg per d of TDCIPP. Nevertheless, serum thyroid stimulating hormone (TSH) levels and the receptor (TSHr) mRNA significantly decreased at only the low dose group. Based on these results, we certified that TDCIPP disturbs the normal bioprocess on TH synthesis, biotransformation or clearance, and hepatic detoxification of pubertal female SD rats, causing thyroid function disorder.

Epidemiological studies have demonstrated that nanometre particles in polluted air can increase the risk of CVD, which is dangerous to mankind. However, little is known regarding the indirect toxic effects on the cardiovascular system of respiratory tract exposure to nanometre particles. As a typical nanomaterial, SWCNTs have gained enormous popularity because of their unique properties. However, increasing attention has been paid to the potential pulmonary toxic effects of respiratory tract exposure to SWCNT than to the potential link of this exposure to cardiovascular disease risk. In this study, a rat intratracheal instillation model was used to evaluate the systemic and secondary effects of respiratory tract exposure to SWCNT, specifically changes in lung tissues, the circulatory system and vascular function. We found increased levels of inflammatory factors and interstitial inflammation in the lungs in this rat model. In addition, up-regulated levels of cytokines and an increase in white blood cells, platelets and fibrinogen were detected in the plasma. These changes were followed by increased blood viscosity in the high dose SWCNT exposure group. In addition, damage to the ultrastructure of the vascular intima in the rats was observed. Changes in coagulation and fibrinolysis activating factors were detected in the plasma. Lower expression of t-PA and higher expression of vWF were observed in the vascular intima of rats exposed to SWCNT at 10.5 and 17.5 mg per kg b.w. for 30 days and 60 days. After exposure to SWCNT for 60 days at 17.5 mg per kg b.w., decreased expression of t-PA gene and increased expression of TM, p38MAPK and PAI-1 genes were observed in the peripheral blood of the rats. Based on these results, we conclude that cardiovascular toxicity caused by respiratory tract exposure to SWCNTs may be induced by indirect effects on vascular homeostasis, which is different from previously reported direct cardiac effects of SWCNT. The present work established a correlation between pulmonary changes and CVD following pulmonary exposure to SWCNT. This study indicates a possible pathophysiological mechanism for CVD caused by pulmonary exposure to SWCNT. More importantly, these results supplement toxicological evaluation data for the risk of CVD caused by respiratory tract exposure to SWCNT.

Background: Carbon nanotube (CNT) mediated drug delivery systems have recently aroused a great deal of interest. Such delivery systems for drugs, proteins and genes have been preliminarily studied using cellular and animal models. For further study of the related biological behaviours of CNTs in vivo, a fast and convenient tracing method is particularly necessary. Methods: We adopted concentrated nitric acid/concentrated sulfuric acid oxidation combined with ultrasonication to treat SWCNTs, then detected and analyzed the samples before and after treatment by transmission electron microscopy (TEM), Fourier transform infrared spectrometry (FT-IR), energy dispersive X-ray spectrometry (EDX) and X-ray photoelectron spectroscopy (XPS). The iodogen oxidative method was used to synthesize iodinated single-walled carbon nanotubes, followed by intratracheal instillation of 125I-labelled SWCNTs to determine their distribution in rats. Results: SWCNTs form more hydroxyl and carboxyl functional groups with no change in their essential characteristics after treatment by violet acid oxidation combined with ultrasonication. 125I can easily form C–I covalent bonds to SWCNTs. The proportion of iodine-125 labelled SWCNTs is 46.14%, the radiochemical purity is 98.95%. In order of total radioactivity concentration in the main organs/tissues and body fluids for 125I-SWCNTs, it was shown that trachea > urine > stomach > small intestine > serum > bladder > blood vessel > kidney > liver > lung > adrenal > femoral head > spleen > testis > thymus > thyroid > heart > fat > muscle > brain. Conclusions: In this paper, we developed a generally adoptable tracing method for studying the biodistribution of SWCNTs (single walled carbon nanotubes) in vivo. SWCNTs could be labelled with radioactive 125I atoms. The 125I labelling method is reliable and effective and affords a quantitative analysis of CNTs accumulated in animal tissues. This result will provide an important reference for future research into the biomedical and pharmacological applications of SWCNTs.

To evaluate the immunotoxicity and effects of noise and/or low‐concentration carbon monoxide (CO) exposure on immune organs and immune functions in rats. 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. 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. 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.