Correlation relationship between cadmium accumulation and histological structures of ovary and uterus in rabbits

Massányi, Péter; Uhrín, V.; Valent, Miroslav

doi:10.1080/10934529709376630

Cited by 10 publications

(11 citation statements)

References 25 publications

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“…Disorders in E 2 secretion may have various causes, including, for example, ovary damage, which was observed in this study and was expressed as, among others, degeneration of the corpus luteum, damaged and less numerous oocytes, and degeneration of the granulosa cells. These effects are in agreement with the literature [20,[28][29][30]. Structural damage to the ovary and disturbed E 2 secretion noted after the highest Cd dose may contribute to the prolongation of the diestrus stage in the estrous cycle.…”

Section: Oxidative Medicine and Cellular Longevitysupporting

confidence: 92%

“…Because of disturbed steroid hormone secretion, it is also suggested that the direct effect of Cd on the ovaries or the indirect effect of Cd on the hypothalamus-pituitarygonadal axis should not be excluded. It was proved in in vivo studies that Cd administration leads to histopathological alterations in the ovary (degeneration of the corpus luteum, damaged and less numerous oocytes, and degeneration of granulosa cells) and uterus (an increase in the luminal epithelial height and in the endometrial thickness) [24,[28][29][30]. In addition, subacute Cd administration led to Cd accumulation and the induction of oxidative stress in rat ovaries and uterus [29,31].…”

Section: Introductionmentioning

confidence: 99%

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Subchronic Exposure to Cadmium Causes Persistent Changes in the Reproductive System in Female Wistar Rats

Nasiadek

Danilewicz

Klimczak

et al. 2019

Oxidative Medicine and Cellular Longevity

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Cadmium (Cd) is an environmental toxicant and endocrine disruptor in humans and animals, and recent studies have illustrated that the uterus is exceedingly sensitive to Cd toxicity. The aim of the study was to investigate the influence of subchronic (90 days) oral Cd exposure in daily doses of 0.09-4.5 mg/kg b.w. on the balance of sex hormones by estimating estradiol (E2) and progesterone (P) concentrations in the uterus and plasma in comparison with the effects of 17β-E2. Additionally, the uterine weight, histopathological changes in the uterus and ovaries, the regularity of the estrous cycle, Cd bioaccumulation in uterine tissue, and selected biochemical parameters of oxidative stress were determined. A long period of observation (three and six months following the administration period) was used to assess whether the existing effects are reversible. The lowest dose of Cd caused effects similar to 17β-E2: an increase of E2 concentration in the uterus, endometrial epithelium thickness, and disturbed estrous cycle with estrus phase prolongation. The obtained results suggest that Cd causes nonlinear response. Higher doses of Cd caused a significant decrease in E2 concentration in the uterus and plasma, estrous cycle disturbances, endometrium atrophy, and structural damage in the ovaries. This dose additionally induces lipid peroxidation in the uterine tissues. It is noteworthy that a prolonged time of observation after terminating the exposure showed persistent changes in the concentration of E2 in uterine tissue, as well as alterations in estrous cycle phases, and an increase in lipid peroxidation in the uterus. Moreover, significant positive correlations between the plasma E2 concentration and endometrial epithelium thickness in all studied groups were found. In summary, subchronic oral Cd exposure of female rats may result in impaired fertility processes.

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Section: Oxidative Medicine and Cellular Longevitysupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Subchronic Exposure to Cadmium Causes Persistent Changes in the Reproductive System in Female Wistar Rats

Nasiadek

Danilewicz

Klimczak

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…In turn, studies on female rats showed that Cd, metal with a very long half-life, accumulates in the female reproductive organs of the hypothalamic-pituitary-gonadal axis (Massányi et al 1995 , 1997 , 2007 ; Varga et al 1993 ; Nasiadek et al 2005 ; Höfer et al 2009 ; Jiménez-Ortega et al 2011 , 2012 ; Rzymski et al 2016 ). The gonadotropins secreted by the anterior pituitary gland are required for synthesis of steroid hormones: estradiol (E 2 ) and progesterone (P).…”

Section: Introductionmentioning

confidence: 99%

“…The review of in vitro and in vivo studies shows that Cd can both increase and inhibit the secretion of the major classes of steroid hormones: E 2 and P and the effects are dependent not only on the dose and route of administration but also on the stages of estrous cycle (Massányi et al 2000 ; Han et al 2006 ; Zhang and Jia 2007 ; Zhang et al 2008 ). Cd also induces significant changes in the structure of ovary (maturation of follicles, follicular atresia, degradation of corpus luteum, the damage of oocytes), as well as the uterus (a significant increase of the uterine epithelium height, interstitial edema, capillary modification) (Paksy et al 1992 ; Massányi and Uhrín 1996 , 1997 ; Massányi et al 1997 , 2005 ; Höfer et al 2009 ; Ali et al 2010 ; Wang et al 2015 ).…”

Section: Introductionmentioning

confidence: 99%

The effect of repeated cadmium oral exposure on the level of sex hormones, estrous cyclicity, and endometrium morphometry in female rats

Nasiadek

Danilewicz

Sitarek

et al. 2018

Environ Sci Pollut Res

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Cadmium (Cd) is regarded as a potential endocrine disruptor. However, the exact mechanism by which this metal may interfere with the reproductive system has not yet been elucidated. The present study aimed to investigate the effect of subacute Cd oral administration at daily doses of 0.09, 1.8, and 4.5 mgCd/kg b.w. and the impact of Cd on sex hormones (estradiol (E2) and progesterone (P)) in the plasma and uterus, as well as on estrous cyclicity and histopathological changes in uterine and ovary in female rats after terminating the exposure and after a prolonged observation period (3 months). Moreover, Cd bioaccumulation in the uterine and brain tissue of rats was analyzed. The study revealed that oral Cd exposure induced changes in the plasma levels of steroid hormones: decrease in E2 and increase in P after the highest dose of Cd. Probably, for the first time, it was evidenced that circulation sex hormone disturbances in Cd-exposed rats caused irregular estrous cycle, persisting for 3 months after exposure termination; no alterations in these hormone levels in uterine tissue were noted. Cd did not induce estradiol-like hyperplasia of endometrium, but resulted in endometrial edema irrespective of the dose, and caused damage of the ovaries after the highest dose. In summary, subacute oral exposure of female rats to Cd may lead to long-term disturbances in reproductive system.

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“…Cd 2# has been reported to accumulate in uterine tissue of rabbit (Massa H nyi et al, 1997) and exert deleterious effect on the rat uterine microcirculation (Copius Peerbom-Stegeman et al, 1987). Insertion of cadmium, nickel, or cobalt wire into one uterine horn of rats on Day 3 of pregnancy has been described to produce a decrease in the number of implants and increase in the number of resorption sites compared with the untreated contralateral horn or to a silver-treated horn.…”

Section: Introductionmentioning

confidence: 99%

In VitroComparative Effect of Cd2+, Ni2+, and Co2+on Mouse Postblastocyst Development

Paksy

Forgács

Gáti

1999

Environmental Research

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Correlation relationship between cadmium accumulation and histological structures of ovary and uterus in rabbits

Cited by 10 publications

References 25 publications

Subchronic Exposure to Cadmium Causes Persistent Changes in the Reproductive System in Female Wistar Rats

Subchronic Exposure to Cadmium Causes Persistent Changes in the Reproductive System in Female Wistar Rats

The effect of repeated cadmium oral exposure on the level of sex hormones, estrous cyclicity, and endometrium morphometry in female rats

In VitroComparative Effect of Cd2+, Ni2+, and Co2+on Mouse Postblastocyst Development

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