Prenatal nicotine exposure induces thymic hypoplasia in mice offspring from neonatal to adulthood

Qu, Wen; Zhao, Wenzhi; Wen, Xiaoru; Yan, Hui-yi; Liu, Hanxiao; Hou, Lifang

doi:10.1016/j.toxlet.2018.12.015

Cited by 10 publications

(8 citation statements)

References 53 publications

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“…Nicotine levels in the amniotic fluid can exceed maternal plasma levels by 88% [8,9]. Perinatal nicotine exposure is harmful to the health of the offspring in many aspects; it results in low birth weight, preterm delivery, stillbirth, neurobehavioral deficits, sudden infant death syndrome, and a range of neuroendocrine, craniofacial, and immune system abnormalities [10][11][12][13][14][15][16]. In addition to these problems, it is especially harmful to the developing respiratory system.…”

Section: Introductionmentioning

confidence: 99%

Comparison of Protective Effects of Electroacupuncture at ST 36 and LU 5 on Pulmonary and Hypothalamic Pituitary Adrenal Axis Changes in Perinatal Nicotine-Exposed Rats

Jiang

Zhao

et al. 2020

BioMed Research International

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Background. Maternal smoking and/or exposure to environmental tobacco smoke continue to be significant factors in fetal and childhood morbidity and are a serious public health issue worldwide. Nicotine passes through the placenta easily with minimal biotransformation, entering fetal circulation, where it results in many harmful effects on the developing offspring, especially on the developing respiratory system. Objectives. Recently, in a rat model, electroacupuncture (EA) at maternal acupoints ST 36 has been shown to block perinatal nicotine-induced pulmonary damage; however, the underlying mechanism and the specificity of ST 36 acupoints for this effect are unknown. Here, we tested the hypothesis that compared with EA at ST 36, EA at LU 5 acupoints, which are on lung-specific meridian, will be equally or more effective in preventing perinatal nicotine-induced pulmonary changes. Methods. Twenty-four pregnant rat dams were randomly divided into 4 groups: saline (“S”), nicotine (“N”), nicotine + ST 36 (N + ST 36), and nicotine + LU 5 (N + LU 5) groups. Nicotine (1 mg/kg, subcutaneously) and EA (at ST 36 or LU 5 acupoints, bilaterally) were administered from embryonic day 6 to postnatal day 21 once daily. The “S” group was injected saline. As needed, using ELISA, western analysis, q-RT-PCR, lung histopathology, maternal and offspring hypothalamic pituitary adrenal axes, offspring key lung developmental markers, and lung morphometry were determined. Results. With nicotine exposure, alveolar count decreased, but mean linear intercept and septal thickness increased. It also led to a decrease in pulmonary function and PPARγ and an increase of β-catenin and glucocorticoid receptor expression in lung tissue and corticosterone in the serum of offspring rats. Electroacupuncture at ST 36 normalized all of these changes, whereas EA at LU 5 had no obvious effect. Conclusion. Electroacupuncture applied to ST 36 acupoints provided effective protection against perinatal nicotine-induced lung changes, whereas EA applied at LU 5 acupoints was ineffective, suggesting mechanistic specificity and HPA axis’ involvement in mediating EA at ST 36 acupoints’ effects in mitigating perinatal nicotine-induced pulmonary phenotype. This opens the possibility that other acupoints, besides ST 36, can have similar or even more robust beneficial effects on the developing lung against the harmful effect of perinatal nicotine exposure. The approach proposed by us is simple, cheap, quick, easy to administer, and is devoid of any significant side effects.

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Section: Introductionmentioning

confidence: 99%

Comparison of Protective Effects of Electroacupuncture at ST 36 and LU 5 on Pulmonary and Hypothalamic Pituitary Adrenal Axis Changes in Perinatal Nicotine-Exposed Rats

Jiang

Zhao

et al. 2020

BioMed Research International

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“…One recent study showed that nicotine hydrogen tartrate administered ad libitum in drinking water to rats (52 ppm nicotine) and mice (514 ppm nicotine) for four weeks induced increased urinary tract cell proliferation (urothelial hyperplasia) [228]. Prenatal exposure of mice to nicotine in vivo induces underdeveloped or involuted thymus (thymic hypoplasia), impairing the immune systems of offspring through adulthood [229]. Cotinine, the major metabolite of nicotine, administered ad libitum in drinking water to rats can induce cell proliferation and hyperplasia in rat urinary bladder and renal tissues, albeit to a lesser degree than nicotine.…”

Section: Mammalian Animalsmentioning

confidence: 99%

A Review of Environmental Pollution from the Use and Disposal of Cigarettes and Electronic Cigarettes: Contaminants, Sources, and Impacts

et al. 2021

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While the impacts of cigarette smoking on human health are widely known, a less recognized impact of tobacco product use and disposal is environmental pollution. This review discusses the current literature related to cigarette and e-cigarette contamination in the context of environmental sources and impacts, with a focus on the documented influences on biota, ranging from bacteria to mammals. Cigarette butts and electronic cigarette components can leach contaminants into soil, water, and air. Cellulose acetate cigarette filters comprising the butts are minimally degradable and are a source of bulk plastic and microplastic pollution, especially in aquatic ecosystems where they tend to accumulate. Cigarette combustion and aerosol production during e-cigarette use result in air contamination from sidestream, exhaled, and thirdhand pathways. The chemical byproducts of tobacco product use contaminate wastewater effluents, landfill leachates, and urban storm drains. The widespread detection of nicotine and cotinine in the environment illustrates the potential for large-scale environmental impacts of tobacco product waste. Studies show that cigarette butt leachate and nicotine are toxic to microbes, plants, benthic organisms, bivalves, zooplankton, fish, and mammals; however, there remain critical knowledge gaps related to the environmental impacts of tobacco product waste on environmental health and ecosystem functioning.

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“…To understand the mechanism of altered inflammation in nicotine-exposed pups, it would be necessary to identify the cells to which nicotine is binding and initiating signaling, and then determining if those cells are the sole source of cytokines or if they work in concert with other cells to elicit an immune response. Although we know that nicotine can cross the placenta and accumulates in the fetal blood and in the breast milk [ 55 , 56 , 57 , 58 , 59 ], it remains unclear whether these significant fetal and neonatal exposures lead to direct changes in the fetal hematopoietic compartment. It is also unknown whether nicotine leads to transient or persisting alterations in developmental hematopoiesis.…”

Section: Does Nicotine Affect Hematopoiesis Via An Altered Inflammatory State?mentioning

confidence: 99%

Clearing the Haze: How Does Nicotine Affect Hematopoiesis before and after Birth?

Cool

Baena

Forsberg

2021

Cancers

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Hematopoiesis is a tightly regulated process orchestrated by cell-intrinsic and cell-extrinsic cues. Over the past several decades, much effort has been focused on understanding how these cues regulate hematopoietic stem cell (HSC) function. Many endogenous key regulators of hematopoiesis have been identified and extensively characterized. Less is known about the mechanisms of long-term effects of environmental toxic compounds on hematopoietic stem and progenitor cells (HSPCs) and their mature immune cell progeny. Research over the past several decades has demonstrated that tobacco products are extremely toxic and pose huge risks to human health by causing diseases like cancer, respiratory illnesses, strokes, and more. Recently, electronic cigarettes have been promoted as a safer alternative to traditional tobacco products and have become increasingly popular among younger generations. Nicotine, the highly toxic compound found in many traditional tobacco products, is also found in most electronic cigarettes, calling into question their purported “safety”. Although it is known that nicotine is toxic, the pathophysiology of disease in exposed people remains under investigation. One plausible contributor to altered disease susceptibility is altered hematopoiesis and associated immune dysfunction. In this review, we focus on research that has addressed how HSCs and mature blood cells respond to nicotine, as well as identify remaining questions.

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Prenatal nicotine exposure induces thymic hypoplasia in mice offspring from neonatal to adulthood

Cited by 10 publications

References 53 publications

Comparison of Protective Effects of Electroacupuncture at ST 36 and LU 5 on Pulmonary and Hypothalamic Pituitary Adrenal Axis Changes in Perinatal Nicotine-Exposed Rats

Comparison of Protective Effects of Electroacupuncture at ST 36 and LU 5 on Pulmonary and Hypothalamic Pituitary Adrenal Axis Changes in Perinatal Nicotine-Exposed Rats

A Review of Environmental Pollution from the Use and Disposal of Cigarettes and Electronic Cigarettes: Contaminants, Sources, and Impacts

Clearing the Haze: How Does Nicotine Affect Hematopoiesis before and after Birth?

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