Damaging effects of polychlorinated biphenyls on chicken primordial germ cells

2002 ◽  
Vol 14 (3) ◽  
pp. 177 ◽  
Author(s):  
Changge Fang ◽  
Caiqiao Zhang ◽  
Guoliang Xia ◽  
Wei Yang

This work describes the effects of a commercial polychlorinated biphenyl (PCB) mixture, Aroclor 1254, as well as 17β-oestradiol (E2) and testosterone on numbers and histomorphological changes of primordial germ cells (PGCs) in gonadal regions of Day 5 Hyline chicken embryos. The oestrogen receptor antagonist, clomiphen, alone or with PCBs was used in an attempt to protect the developing gonad from oestrogen-like effects of chemical PCBs. The results were as follows: (i) PCBs delayed embryonic development independently of dose (1�µg/eggP<0.05; 10 µg/eggP<0.01; 100 µg/eggP<0.001 v. the control) and caused a dose-independent increase in mortality compared with the control group (10 µg/egg P<0.01; 100 µg/eggP<0.05); maximal mortality was observed in the 1 µg/eggP<0.001); (ii) PCBs decreased PGC numbers dose dependently (P<0.001) and caused a swollen nucleus with hyperchromatism (pyknosis) or cytoplasm vacuolation as signs of gonadal PGC degeneration in all PCB groups, or even complete disappearance in the 100 µg/eggiii) after PCB treatment, the index of gonadal lesion increased significantly with the decrease of gonadal PGC number (1, 10 and 100 µg/eggP<0.001); (iv) there were no observed effects of E2, testosterone and clomiphen on PGCs in the experiments; and (v) clomiphen failed to block the damaging effects of PCBs. These results suggest that the adverse effects of PCBs on chicken gonadal and germ cell development were initiated during the early stages of incubation through direct toxic effects, rather than through oestrogen-mimicking actions. As PGC numbers in the gonads decrease and the index of gonadal lesion increases, one may expect reproductive function to be compromised.

2019 ◽  
Vol 242 (1) ◽  
pp. T51-T68 ◽  
Author(s):  
Patrycja A Jazwiec ◽  
Deborah M Sloboda

It is well established that early life environmental signals, including nutrition, set the stage for long-term health and disease risk – effects that span multiple generations. This relationship begins early, in the periconceptional period and extends into embryonic, fetal and early infant phases of life. Now known as the Developmental Origins of Health and Disease (DOHaD), this concept describes the adaptations that a developing organism makes in response to early life cues, resulting in adjustments in homeostatic systems that may prove maladaptive in postnatal life, leading to an increased risk of chronic disease and/or the inheritance of risk factors across generations. Reproductive maturation and function is similarly influenced by early life events. This should not be surprising, since primordial germ cells are established early in life and thus vulnerable to early life adversity. A multitude of ‘modifying’ cues inducing developmental adaptations have been identified that result in changes in reproductive development and impairments in reproductive function. Many types of nutritional challenges including caloric restriction, macronutrient excess and micronutrient insufficiencies have been shown to induce early life adaptations that produce long-term reproductive dysfunction. Many pathways have been suggested to underpin these associations, including epigenetic reprogramming of germ cells. While the mechanisms still remain to be fully investigated, it is clear that a lifecourse approach to understanding lifetime reproductive function is necessary. Furthermore, investigations of the impacts of early life adversity must be extended to include the paternal environment, especially in epidemiological and clinical studies of offspring reproductive function.


2018 ◽  
Vol 99 (6) ◽  
pp. 980-985
Author(s):  
Yu A Dudareva ◽  
I P Saldan ◽  
Ya N Shoykhet ◽  
V I Kiselev ◽  
V A Gur'eva

Aim. To determine the possible damaging effects of ecologically unfavorable environmental factors (radiation and chemical) on the health of descendants. Methods. The cross-sectional study included 232 women of the Altai territory, who were divided into three groups: the first group included the descendants of persons who were in the area of radiation exposure, the second one - the descendants of chemical workers, the third group was the control group. As part of the expedition trip to the study areas, the collection of clinical and anamnestic data, the study of extragenital, gynecological morbidity, laboratory and functional methods of research were carried out. Results. The data were obtained confirming the most damaging effect on reproductive health in the descendants of persons who were in the area of radiation exposure. It was the first group where the high frequency of extragenital and gynecological pathology was revealed. At the same time, the reproductive function of women, closely related to functional changes in the immune system, was disordered. The results of the study of a number of parameters of the immune system revealed changes in the functioning of cellular immunity, increase in the level of proinflammatory cytokines (tumor necrosis factor), mainly in the descendants of persons who were in the area of radiation exposure, in contrast to the descendants of workers of chemical production and control group. Conclusion. A comparative assessment of some health parameters of descendants of persons exposed to radiation and chemical factors showed that the most damaging effect on the reproductive health of descendants is caused by radiation factor.


Author(s):  
Amreek Singh ◽  
Warren G. Foster ◽  
Anna Dykeman ◽  
David C. Villeneuve

Hexachlorobenzene (HCB) is a known toxicant that is found in the environment as a by-product during manufacture of certain pesticides. This chlorinated chemical has been isolated from many tissues including ovary. When administered in high doses, HCB causes degeneration of primordial germ cells and ovary surface epithelium in sub-human primates. A purpose of this experiment was to determine a no-effect dose of the chemical on the rat ovary. The study is part of a comprehensive investigation on the effects of the compound on the biochemical, hematological, and morphological parameters in the monkey and rat.


1998 ◽  
Vol 69 (10) ◽  
pp. 911-915 ◽  
Author(s):  
Tamao ONO ◽  
Ryohei YOKOI ◽  
Seishi MAEDA ◽  
Takao NISHIDA ◽  
Hirohiko AOYAMA

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