• 제목/요약/키워드: reproduction and development toxicity

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토양선충 Caenorhabditis elegans를 이용한 Nonylphenol의 독성 영향 연구 (Toxicological Study on Nonylphenol using the Soil Nematode, Caenorhabditis elegans)

  • 노지연;최진희
    • Environmental Analysis Health and Toxicology
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    • 제21권4호
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    • pp.323-330
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    • 2006
  • The aim of current study was to evaluate the toxicity of nonylphenol(NP) on soil nematode, Caenorhabditi elegans. The stress-related gene expression, growth, reproduction and development have been employed to monitor soil toxicity. The 24-h median effect concentrations $(LC_{50s})$ of NP was $0.15mg/L$. The expressions of vitellogenin-6, vitellogenin-2, cytochrome P450 family protein 35a2 and apoptosis enhancer-1 genes were upregulated in C. elegans by NP exposure. Alterations in growth, reproduction and development were also observed in NP-exposed group and especially hatching failure was observed. The overall results indicate that C. elegans has considerable potential as sensitive markers for NP toxicity monitoring.

Arsenic Toxicity in Male Reproduction and Development

  • Kim, Yoon-Jae;Kim, Jong-Min
    • 한국발생생물학회지:발생과생식
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    • 제19권4호
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    • pp.167-180
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    • 2015
  • Arsenic is a toxic metalloid that exists ubiquitously in the environment, and affects global health problems due to its carcinogenicity. In most populations, the main source of arsenic exposure is the drinking water. In drinking water, chronic exposure to arsenic is associated with increased risks of various cancers including those of skin, lung, bladder, and liver, as well as numerous other non-cancer diseases including gastrointestinal and cardiovascular diseases, diabetes, and neurologic and cognitive problems. Recent emerging evidences suggest that arsenic exposure affects the reproductive and developmental toxicity. Prenatal exposure to inorganic arsenic causes adverse pregnancy outcomes and children's health problems. Some epidemiological studies have reported that arsenic exposure induces premature delivery, spontaneous abortion, and stillbirth. In animal studies, inorganic arsenic also causes fetal malformation, growth retardation, and fetal death. These toxic effects depend on dose, route and gestation periods of arsenic exposure. In males, inorganic arsenic causes reproductive dysfunctions including reductions of the testis weights, accessory sex organs weights, and epididymal sperm counts. In addition, inorganic arsenic exposure also induces alterations of spermatogenesis, reductions of testosterone and gonadotrophins, and disruptions of steroidogenesis. However, the reproductive and developmental problems following arsenic exposure are poorly understood, and the molecular mechanism of arsenic-induced reproductive toxicity remains unclear. Thus, we further investigated several possible mechanisms underlying arsenic-induced reproductive toxicity.

Isoprocarb induces acute toxicity in developing zebrafish embryos through vascular malformation

  • Park, Hahyun;Song, Gwonhwa;Lim, Whasun
    • 한국동물생명공학회지
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    • 제36권1호
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    • pp.17-24
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    • 2021
  • In this study, the potential toxicity of isoprocarb was demonstrated using zebrafish embryos. We treated isoprocarb (0, 29, and 58 mg/L) to the zebrafish embryos for 72 h then, we estimated morphological changes and apoptotic cell numbers. The increasing extent of apoptosis from the anterior to posterior region of developing zebrafish larvae was correlated with toxicity in the overall development process, including growth and normal organ formation. The appearance of abnormalities in the isoprocarb-treated groups in comparison to normal developing zebrafish larvae was verified using quantitative image analysis based on ImageJ software program. The vascular system comprising a complex interconnection of blood vessels was visualized in vessel-fluorescent transgenic zebrafish (fli1:eGFP). The main vasculature was malformed on isoprocarb treatment, and this was also related to cardiac defects. Taken together, normal embryonic development in zebrafish was interrupted owing to the acute toxicity of isoprocarb.

Endocrine Disruptors in Developing Embryo on Daphnia magna

  • Kim, Pan-Gyi;Hwang, Seong-Hee
    • 한국환경보건학회지
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    • 제28권4호
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    • pp.17-22
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    • 2002
  • In crustaceans, as in other arthropods, the molt cycle and the physiological process of growth are controlled by molting hormones (MH) which are steroid hormones, the ecdysteroids. Ecdysteroids are major arthropod hormones which control both development (embryonic and larval molts, metamorphosis) and reproduction. The purpose of the present study was to evaluate both fenarimol and methoprene for embryotoxicity to daphnids. The embryotoxicity associated with each compound was assessed to discern whether the embryotoxicity of methoprene might be due to ecdysone agonist and the ecdysone antagonistic effects of fenarimol on Daphnia embryo. Exposure of daphnids for three weeks to 50 M methoprene resulted in a significantly high incidence of offspring that exhibited general toxicity. This exposure concentration had significant effects on the overall number of embryo death. However, exposure to 3 or 1 $\mu$M fenarimol were no significant effects on the embryo toxicity. The incidence of both of these toxicity increased with methoprene exposure. This observation suggest that methoprene showed embryonic general toxicity during embryo development, while, only fenarimol showed weak general toxicity with early stages of embryonic development.

Mecoprop-p interrupts the development of zebrafish via apoptosis and vascular damage

  • Park, Junho;An, Garam;Park, Hahyun;Hong, Taeyeon;Song, Gwonhwa;Lim, Whasun
    • 한국동물생명공학회지
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    • 제37권3호
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    • pp.162-168
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    • 2022
  • Mecoprop-p, a chlorophenoxy herbicide, has been widely used since the 1980s. Due to its high water solubility, it could be detected in the aquatic environment, as it has already been detected in the surface water or groundwater in several countries. The toxicity of other chlorophenoxy herbicides has been reported; however, there are few studies on the toxicity of mecoprop-p, one of the chlorophenoxy herbicides, on aquatic organisms. Here, we investigated the toxic effects of mecoprop-p using zebrafish. After mecoprop-p exposure, we observed that the zebrafish larvae eyes did not form normally, heart edema was generated, and the body length was shortened. The number of cells undergoing apoptosis also increased in the anterior part including head, heart, and yolk sac of the mecoprop-p-treated zebrafish compared to the untreated controls. Moreover, cardiovascular structures, including the heart and aortic arches, were also malformed after exposure to mecoprop-p. Therefore, our results suggest that mecoprop-p could cause abnormal development in zebrafish larvae and there is also a high possibility that mecoprop-p would be toxic to other aquatic organisms.

치매 치료제 염산 디히드로에보다이아민의 생식 및 발생 독성 (Reproduction and Development Toxicity of Anti-Alzheimer′s Drug Dehydroevodiamine-HCl)

  • 성이숙;정성윤;서영득;진미령;최봉웅;장병모;김대경
    • 약학회지
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    • 제46권6호
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    • pp.452-458
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    • 2002
  • Dehydroevodiamine-HCl (DHED), which is a component separated from Evodia rutaecarpa Bentham, has novel anticholinesterase and antiamnesic activities in a scopolamine-induced amnesia model. Several studies suggest that DHED might be an effective drug for Alzheimer's disease and a vascular type of dementia. DHED was at dose levels of 0, 50, 100 and 200 mg/kg/day administered intraperitoneally to Sprague-Dawley male rats for 60 days before mating and to females from 14 days before mating to 7 days after mating. Effects of the DHED on general symptom and reproductive performance of parent animals and embryonic development were examined. In male parents, whereas no death was observed, reduction in the increase rate of body weight was found at 200 mg/kg. In female parents, both of the mating performance and the fertility of parent animals were decreased at 200 mg/kg, but not significantly. In 200 mg/kg treated group, the fetal death rate was increased but total fetuses showed no changes compared to the control group. There were no malformed F1 fetuses in all groups.

Di-(2-ethylhexyl) Phthalate (DEHP) and Uterine Histological Characteristics

  • Cheon, Yong-Pil
    • 한국발생생물학회지:발생과생식
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    • 제24권1호
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    • pp.1-17
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    • 2020
  • Phthalates and those metabolites have long history in industry and suspected to have deficient effects in development and reproduction. These are well-known anti-androgenic chemicals and many studies have examined the effects of these compounds on male reproduction as toxins and endocrine disruptors. Uterus is a key organ for proper embryo development, successful reproduction, and health of eutherian mammals including women. To understand the effects of the phthalate, the horizontal approach with a whole group of phthalate is best but the known phthalates are huge and all is not uncovered. Di-(2-ethylhexyl) phthalate (DEHP) is the most common product of plasticizers in polymer products and studied many groups. Although, there is limited studies on the effects of phthalates on the female, a few studies have proved the endocrine disrupting characters of DEHP or phthalate mixture in female. An acute and high dose of DEHP has adverse effects on uterine histological characters. Recently, it has been revealed that a chronical low-dose exposing of DEHP works as endocrine disrupting chemicals (EDC). DEHP can induce various cellular responses including the expression regulation of steroid hormone receptors, transcription factors, and paracrine factors. Interestingly, the response of uterus to DEHP is not monotonous and the exposed female has various phenotypes in fertility. These suggest that the exposing of DEHP may causes of histological modification in uterus and of disease in female such as endometriosis, hyperplasia, and myoma in addition to developmental and reproductive toxicity.

Epichlorohydrin의 유해성과 작업환경 관리 (Hazards Assessment and Workplace Management of Epichlorohydrin)

  • 김현영;황양인;국원근
    • 한국산업보건학회지
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    • 제22권2호
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    • pp.164-173
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    • 2012
  • Objectives: Epichlorohydrin is a material that has been predicted to have high volatility and strong toxicity and is used normally in working area. Therefore, the hazardous and dangerous level and the foreign management system about epichlorohydrin should be invested at home and abroad and through hazard assessment for occupational environment measurement and exposure status of industrial workers in domestic working area. Methods: To assess risk and to suggest Development and Adoption to prevent health damage of workers owing to the epichlorohydrin exposure, the hazardousness and dangerousness of epichlorohydrin and its practical examples and regulation level for domestic and abroad health impairment are researched on the base of various references. Results: The epichlorohydrin caused skin and mucus membrane irritation, respiratory paralysis, kidney and live damage under the influence of acute toxicity and in animal study, it was confirmed as a doubtful carcinogenic substance to trigger reducement of sperm number and reproduction ability, abnormal spermatogenesis, mutagen, increase of forestomach epithelium and occurrence of papilloma and so on, as well as it induced stimulus asthma and allergic contact dermatitis for exposure workers. Conclusions: Epichlorohydrin was found to occur allergic contact dermatitis, carcinogenesis doubt and reproduction toxicity and was verified as a material which would be established reinforcement of management level to care health of handlers, such as denotement dangerousness of skin absorption.

Anti-Developmental Effects of Imazosulfuron on Zebrafish Embryos During Development

  • Park, Sunwoo;Song, Gwonhwa;Lim, Whasun
    • 한국동물생명공학회지
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    • 제35권1호
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    • pp.28-34
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    • 2020
  • Imazosulfuron is globally considered as a relatively safe herbicide that controls plant growth by interfering with amino acid synthesis. It is stable, persists in the soil, and has low toxicity; however, studies about the toxic effects of imazosulfuron on non-targeted aquatic vertebrates are scarce. In this study, imazosulfuron was able to induce acute lethality on zebrafish embryos within 48 h. Imazosulfuron also had adverse effects on heartbeats and induced abnormal development with pericardial edema and scoliosis. Moreover, apoptosis and oxidative stress were increased by imazosulfuron in a dose-dependent manner. Thus, all our results showed that imazosulfuron has toxic effects on zebrafish embryogenesis.

Cadmium exposure impairs porcine embryonic development by inducing oxidative stress and mitochondrial dysfunction

  • Min Ju Kim;Se‑Been Jeon;Hyo‑Gu Kang;Bong‑Seok Song;Bo‑Woong Sim;Sun‑Uk Kim;Pil‑Soo Jeong;Seong‑Keun Cho
    • 한국동물생명공학회지
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    • 제39권1호
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    • pp.48-57
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    • 2024
  • Background: Cadmium (Cd) is toxic heavy metal that accumulates in organisms after passing through their respiratory and digestive tracts. Although several studies have reported the toxic effects of Cd exposure on human health, its role in embryonic development during preimplantation stage remains unclear. We investigated the effects of Cd on porcine embryonic development and elucidated the mechanism. Methods: We cultured parthenogenetic embryos in media treated with 0, 20, 40, or 60 µM Cd for 6 days and evaluated the rates of cleavage and blastocyst formation. To investigate the mechanism of Cd toxicity, we examined intracellular reactive oxygen species (ROS) and glutathione (GSH) levels. Moreover, we examined mitochondrial content, membrane potential, and ROS. Results: Cleavage and blastocyst formation rates began to decrease significantly in the 40 µM Cd group compared with the control. During post-blastulation, development was significantly delayed in the Cd group. Cd exposure significantly decreased cell number and increased apoptosis rate compared with the control. Embryos exposed to Cd had significantly higher ROS and lower GSH levels, as well as lower expression of antioxidant enzymes, compared with the control. Moreover, embryos exposed to Cd exhibited a significant decrease in mitochondrial content, mitochondrial membrane potential, and expression of mitochondrial genes and an increase in mitochondrial ROS compared to the control. Conclusions: We demonstrated that Cd exposure impairs porcine embryonic development by inducing oxidative stress and mitochondrial dysfunction. Our findings provide insights into the toxicity of Cd exposure on mammalian embryonic development and highlight the importance of preventing Cd pollution.