Maternal exposure to di(2-ethylhexyl) phthalate (DEHP) causes multigenerational adverse effects on the uterus of F1 and F2 offspring rats.

Shanmugam, Dharani Abirama Sundari; Dhatchanamurthy, Sakthivel; Leela, Kamakshi Arjunan; Bhaskaran, Ravi Sankar

doi:10.1016/j.reprotox.2022.11.006

Cited by 14 publications

(5 citation statements)

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“…Phthalate esters are also active in the female reproductive system, with DEHP affecting ovarian function, which causes decreased serum estradiol concentrations, prolonged estrous cycles and failure of ovulation and cystic progression [ 6 ]. Maternal exposure to DEHP resulted in reproductive toxicity and led to modulation in the abundance of molecules that regulate uterine function in the following generation of rats [ 95 ]. The MEHP compound (monoethylhexyl phthalate), the active metabolite of DEHP, is assumed to be able to suppress aromatase in granulosa cells through the activation of PPARs (peroxisome proliferator-activated receptors).…”

Section: Effects Of Bisphenol a And Other Additives On Fertility And ...mentioning

confidence: 99%

Impact of Microplastics and Nanoplastics on Livestock Health: An Emerging Risk for Reproductive Efficiency

Urli

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Crociati

et al. 2023

Animals

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Pollution due to microplastics and nanoplastics is one of the major environmental issues of the last decade and represents a growing threat to human and animal health. In aquatic species, there is a large amount of information regarding the perturbation of marine organisms; instead, there are only a few studies focusing on the pathophysiological consequences of an acute and chronic exposure to micro- and nanoplastics in mammalian systems, especially on the reproductive system. There are several studies that have described the damage caused by plastic particles, including oxidative stress, apoptosis, inflammatory response, dysregulation of the endocrine system and accumulation in various organs. In addition to this, microplastics have recently been found to influence the evolution of microbial communities and increase the gene exchange, including antibiotic and metal resistance genes. Special attention must be paid to farm animals, because they produce food such as milk, eggs and meat, with the consequent risk of biological amplification along the food chain. The results of several studies indicate that there is an accumulation of microplastics and nanoplastics in human and animal tissues, with several negative effects, but all the effects in the body have not been ascertained, especially considering the long-term consequences. This review provides an overview of the possible adverse effects of the exposure of livestock to micro- and nanoplastics and assesses the potential risks for the disruption of reproductive physiological functions.

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Section: Effects Of Bisphenol a And Other Additives On Fertility And ...mentioning

confidence: 99%

Impact of Microplastics and Nanoplastics on Livestock Health: An Emerging Risk for Reproductive Efficiency

Urli

Pause

Crociati

et al. 2023

Animals

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“…The uterus is a crucial target organ in mammalian development in terms of sexual maturation, and uterine cells respond to estrogen and progesterone for the regulation of endometrial cell proliferation and differentiation ( 15 ). Exposure to DEHP can alter the number of endometrial glands and disrupt their structure in rats and mice ( 17 , 18 , 56 ).…”

Section: Discussionmentioning

confidence: 99%

“…The research findings indicate that exposure to DEHP in animal experiments is linked to reduced gene expression and expression of critical proteins. This exposure may contribute to the development of defects, such as abnormal uterine structure, epithelial proliferation, uterine receptivity, and endometrial shedding in rats ( 17 , 18 ). These results highlight the potential adverse effects of DEHP exposure on reproductive health and provide insight into the mechanisms by which DEHP affects the reproductive system.…”

Section: Introductionmentioning

confidence: 99%

Phthalates exposure and pubertal development in a 15-year follow-up birth cohort study in Taiwan

Huang

Wang

et al. 2023

Front. Endocrinol.

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PurposePhthalates are ubiquitous endocrine disruptors that can affect pubertal development in children. The association of fetal and childhood levels of phthalates with pubertal development were explored.MethodsWe conduct a population-based birth cohort study to investigate the association between prenatal and childhood exposure to phthalates and pubertal development. Initially, a total of 445 children were recruited from 2000 to 2001, of which 90 children were followed for 15 years which measurements of urine and development assessed at 2, 5, 8, 11, and 14 years. We defined higher Tanner stage as the 14-year-old Tanner stage ≥ 4 and 5 for boys and girls, respectively. A logistic regression analysis was conducted to estimate the crude and adjusted odds ratio of a higher Tanner stage at 14 years old. The Pearson correlation coefficient and multiple linear regression were used to estimate the association of testicular volume, uterine volume, ovarian volume, and blood hormones at 14 years of age with the log-transformed concentration of phthalates at 2, 5, 8, 11, and 14 years.ResultsIn boys, a significantly different geometric mean of mono-benzyl phthalate (MBzP) was observed in 11-year-olds; 6.82 and 2.96 in the lower Tanner stage group and higher Tanner stage group. In girls, a significant difference in the geometric mean of mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) in 11-year-olds and mono-ethyl phthalate (MEP) in 2-year-olds was observed; MEHHP was 32.97 and 18.13 in the lower Tanner stage group and higher Tanner stage group, and MEP was 26.54 and 65.74 in the lower Tanner stage group and higher Tanner stage group, respectively. Uterine volume at 14 years old was negatively associated with several phthalate metabolites (MEHP at 8 years old, MnBP at 8 years old, MBzP at 14 years old, MMP prenatally, MMP at 8 years old, and MEP at 8 years old) after adjusting for covariates. However, no significant correlations were found between phthalate metabolites and ovarian or testicular volume.ConclusionPhthalate exposure at certain time points may influence the reproductive development of children during puberty; however, further studies should be conducted to determine the causal nature of this association.

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“…Such widespread reproductive toxicants as bisphenols and phthalate esters are known to induce oxidative DNA damage in both the male and female germ line [ 114 , 115 , 116 , 117 , 118 ] and are acknowledged mutagens [ 119 , 120 ]. These compounds also induce multigenerational infertility in animal models [ 121 , 122 , 123 ], strongly suggesting they are capable of leaving an indelible mark of the future fertility of our species through a combination of genetic and epigenetic effects [ 124 , 125 ].…”

Section: Is Fecundity Changing?mentioning

confidence: 99%

The Global Decline in Human Fertility: The Post-Transition Trap Hypothesis

Aitken

2024

Life

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Over the past half a century many countries have witnessed a rapid fall in total fertility rates, particularly in the world’s most advanced economies including the industrial powerhouses of Eastern Asia and Europe. Such nations have now passed through the first and second demographic transitions and are currently exhibiting fertility rates well below the replacement threshold of 2.1, with no sign of recovery. This paper examines the factors responsible for driving these demographic transitions and considers their impact on both fertility and fecundity (our fundamental capacity to reproduce). I argue that because the first demographic transition was extremely rapid and largely driven by socioeconomic factors, it has had no lasting impact on the genetic/epigenetic underpinnings of human fecundity. However, the second demographic transition will be different. A series of conditions associated with low fertility societies, including relaxed selection pressure for high-fertility genotypes, the indiscriminate use of assisted reproductive technologies to treat human infertility, and environmental contamination with reproductive toxicants, may impact our genetic constitution in ways that compromise the future fecundity of our species. Since any fundamental change in the genetic foundations of human reproduction will be difficult to reverse, we should actively pursue methods to monitor human fecundity, as sub-replacement fertility levels become established across the globe.

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Maternal exposure to di(2-ethylhexyl) phthalate (DEHP) causes multigenerational adverse effects on the uterus of F1 and F2 offspring rats.

Cited by 14 publications

References 85 publications

Impact of Microplastics and Nanoplastics on Livestock Health: An Emerging Risk for Reproductive Efficiency

Impact of Microplastics and Nanoplastics on Livestock Health: An Emerging Risk for Reproductive Efficiency

Phthalates exposure and pubertal development in a 15-year follow-up birth cohort study in Taiwan

The Global Decline in Human Fertility: The Post-Transition Trap Hypothesis

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