• Title/Summary/Keyword: developmental toxicity

검색결과 190건 처리시간 0.031초

랫드 전배아배양법을 이용한 2-Bromopropane의 최기형성 평가 (Teratogenicity Evaluation of 2-Bromopropane Using Rat Whole Embryo Culture)

  • 김종춘;신동호;김성호;양영수;오기석;강성철;정문구
    • Toxicological Research
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    • 제22권2호
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    • pp.127-133
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    • 2006
  • Recently, we have reported that the environmental pollutant 2-bromopropane (2-BP) induces a significant embryo-fetal developmental toxicity in rats. However, the cause of developmental toxicity and the relationship between maternal and developmental toxicities could not be elucidated because the developmental toxicity of 2-BP was observed only in the presence of maternal toxicity The in vitro teratogenicity study using whole embryo culture was carried out to understand the teratogenic properties and the possible mechanism of teratogenicity induced by 2-BP in rats. Rat embryos aged 9.5 days were cultured in vitro for 48 hrs at medium concentrations of 0, 1, 3, or 10 mg/ml of 2-BP. Embryos were evaluated for growth, differentiation, and morphological alterations at the end of the culture period. At 10 mg/ml, 2-BP caused a delay in the growth and differentiation of embryos and an increase in the incidence of morphological alterations, including altered yolk sac circulation, abnormal axial rotation, craniofacial hypoplasia, open neuropore, absent optic vesicle and kinked somites. At 3 mg/ml, only a delay in the growth and differentiation of embryos was observed. There were no adverse effects on embryonic growth and development at the concentration of 1 mg/ml. The results showed that the exposure of 2-BP to rat embryos results in a developmental delay and morphological alterations at dose levels of 3 mg/ml culture media or higher and that 2-BP can induce a direct developmental toxicity in rat embryos.

Assessment on combined repeated dose and reproduction/developmental toxicity of benzoyl peroxide

  • Sanghwan Song;Kim, Su-Hyon;Heekyung Bae;Lee, Moon-Soon;Park, Kwangsik
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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    • pp.171-171
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    • 2002
  • This study was carried out by an Korean GLP laboratory to assess the combined repeated dose, reproduction and developmental toxicity of benzoyl peroxide for OECD SIDS(Screening Information Data Set) program. Male and female Sprague Dawley rats were exposed to benzoyl peroxide at levels of 0, 250, 500 and 1,000 mg/kg/day for 29 days for male and for 41-51 days for female.(omitted)

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발달 독성학에서 비대칭 로짓 모형을 사용한 이진수 자료와 연속형 자료에 대한 결합분석 (Joint analysis of binary and continuous data using skewed logit model in developmental toxicity studies)

  • 김영화;황범석
    • 응용통계연구
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    • 제33권2호
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    • pp.123-136
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    • 2020
  • 하나의 개체에서 여러가지 측정치가 동시에 관찰되는 경우는 다양한 연구 분야에서 흔히 나타난다. 발달 독성학 연구에서는 특정 독성 물질의 각기 다른 수준에 노출된 임신한 어미 쥐에 대해 기형인 태아의 존재와 태아의 무게가 동시에 측정된다. 이런 두 변수를 결합하여 모형화하는 것은 각기 독립적인 두 모형으로 분석하는 것보다 더 효율적인 결과를 낸다고 알려져 있다. 대부분의 결합 모형은 정규분포를 랜덤효과로 가정하여 분석한다. 그러나 발달 독성학 연구에서처럼 반응변수들의 분포가 독성 물질이 변함에 따라 불규칙하게 변하는 경우 정규분포의 가정으로는 그 특징을 잡아낼 수 없게 된다. 본 논문에서는 이진수 자료와 연속형 자료에 대해 비대칭 로짓 모형을 사용한 베이지안 결합모형을 제시한다. 본 모형은 비대칭 로짓 모형을 사용함으로써 반응변수의 분포의 형태가 독성 물질의 수준에 따라 대칭/비대칭의 형태를 자유롭게 띨 수 있는 장점을 가지고 있다. 모형의 적합성을 살펴보기 위해 발달 독성학 연구에서 독성 물질 DEHP에 적용하여 그 결과를 확인해본다.

Assessing systemic, developmental, and reproductive toxicity and estrogenicity of Korean red ginseng extract G1899 in juvenile Sprague-Dawley Rats

  • Sangyun Kim;Ji-Seong Jeong;Woojin Kim;Onju Ham;Yixian Quah;Soontag Jung;Dong-Ju Park;Min Jae Kim;Byung-Cheol Han;Eunji Kim;Seung-Jin Lee;Wook-Joon Yu
    • Journal of Ginseng Research
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    • 제48권3호
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    • pp.333-340
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    • 2024
  • Background: Korean red ginseng (KRG) is a product from ginseng roots, which is enriched with ginsenosides and has been utilized for a long time as an adaptogen to alleviate various physiological or disease conditions. While KRG is generally considered safe, conducting a thorough toxicological assessment of the spray-dried powder G1899 during the juvenile period is essential to establish its safety profile. This study aimed to assess the safety of G1899 during the juvenile period using Sprague-Dawley rats. Methods: Two studies were conducted separately: a juvenile toxicity study and a uterotrophic bioassay. To assess the potential toxicity at systemic, postnatal developmental, and reproductive levels, G1899 was orally gavaged once a day in post-weaning juvenile Sprague-Dawley (SD) rats at 0, 1250, 2500, or 5000 mg/kg/day. Estrogenicity was assessed by orally gavaging G1899 in immature female SD rats at 0, 2500, or 5000 mg/kg/day on postnatal days (PND) 19-21, followed by a uterotrophic bioassay. These studies were conducted in accordance with the Good Laboratory Practice (GLP) regulations and regulatory test guidelines. Results: Regarding juvenile toxicity, no abnormalities related to the G1899 treatment were observed in any group during the experiment. Moreover, no uterotrophic responses were observed in the dosed female group. Based on these results, the no observed adverse effect level (NOAEL) of G1899 was determined to be at least 5000 mg/kg/day for general systemic function, developmental/reproductive function, and estrogenic activity. Conclusion: Our results suggest that G1899 is not toxic to juveniles at doses of up to 5000 mg/kg/day.

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.

금붕어 수정난의 2,3,7,8-TCDD 노출에 따른 다이옥신 관련 유전자의 발현 및 형태학적 변화 (Early Life Stage Toxicity of 2,3,7,8,-Tetrachlorodibenzop-Dioxin(TCDD) in Goldfish(Carassius auratus))

  • 오승민;유병택;김하룡;정규혁
    • Environmental Analysis Health and Toxicology
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    • 제24권1호
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    • pp.1-8
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    • 2009
  • In this study, we obtained the fertilized eggs from goldfish(Carassius auratus) and observed normal developmental stage(from fertilized eggs to larvae) in non-exposed groups. Goldfish embryos at 3 h postfertilization(hpf) were statically exposed for 1 h to either dimethylsufoxide(DMSO, 0.1%, v/v) or TCDD($0.5{\mu}g/L$). Toxicity and morphological changes were characterized from 3 to 120 h postfertilization(hpf). Egg mortality($0{\sim}48$ hpf) and hatching ratio($72{\sim}83$ hpf) in TCDD-exposed group were significantly different from control groups. However, pericardial edema was first observed at 72 hpf, followed by the onset of yolk sac edema and mortality. In addition, goldfish embryos-larvae exposed to TCDD significantly increased TCDD-related gene such as CYP1A($24{\sim}72$ hpf) and AhR2(72 hpf). This is the first study about in-depth characterization of TCDD-induced developmental toxicity in goldfish(Carassius auratus).

랫드에 미치는 Permethrin의 발생독성에 관한 연구 (Effect of Permethrin on Embryonic Developments in Rats)

  • 윤효정;정문호
    • 한국환경보건학회지
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    • 제31권4호
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    • pp.254-259
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    • 2005
  • Permethrin, a synthetic pyrethroid insecticide, has been widely used to protect domestic animals and the public health, as well as in agriculture against a variety of pests, which provides potential for environmental exposure. Permethrin is classified as possible human carcinogen and endocrine disrupting chemical by many international authorities. However, its developmental effects have been rarely studied. This study investigated the effects of permethrin during embryo-genesis. Developmental toxicity of permethrin was evaluated using short-term in vitro battery system. Gestation day 9.5 rat embryos (organogenesis) were cultured with permethrin (0.1,0.4 and 0.8 mg/ml) for 48 hours using whole embryo culture system. All the treatments exhibited significant decreases in the total morphological score. Permethrin induced significant growth retardation and the developmental abnormality at doses of 0.4 and 0.8 mg/ml. Moreover, the DNA and protein contents of embryos decreased in dose-dependent manner. These observations suggest that permethrin contributes to toxicity on embryonic developments in rats.

Norflurazon causes developmental defects including cardiovascular abnormalities in early-stage zebrafish (Danio rerio)

  • An, Garam;Park, Hahyun;Hong, Taeyeon;Song, Gwonhwa;Lim, Whasun
    • 한국동물생명공학회지
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    • 제37권3호
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    • pp.176-182
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    • 2022
  • Norflurazon is widely used on agricultural lands and has a high potential to pollute water sources. However, its effects on fish have not been fully elucidated. The purpose of our study was to determine whether norflurazon adversely affects the developmental stage of zebrafish, which are frequently used as a model system to evaluate the environmental impact of pollutants. Norflurazon interfered with the hatching of zebrafish embryos and induced several sublethal deformities including body length reduction, increased yolk sac volume, and enlargement of the pericardial region. We further examined the cardiotoxicity of norflurazon in the flk1:eGFP transgenic zebrafish line. The vascular network, mainly in the brain region, was significantly disrupted in norflurazon-exposed zebrafish. In addition, due to the failure of cardiac looping, norflurazon-exposed zebrafish had an abnormal cardiac structure. These developmental abnormalities were related to the apoptotic process triggered by norflurazon. Overall, the present study demonstrated the non-target toxicity of norflurazon by analyzing the hazardous effects of norflurazon on developing zebrafish.