2012
DOI: 10.1016/j.etp.2010.06.001
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Effects of arsenic exposure during the pre- and postnatal development on the puberty of female offspring

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Cited by 32 publications
(9 citation statements)
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“…The VO day and occurrence of the first estrus are markers of this event (Guyton & Hall, , 1996). In the present work, both parameters were delayed in females after prenatal arsenic exposure corroborating the findings of Dávila-Esqueda et al (2012) in female rats exposed to 3 ppm sodium arsenite in drinking water from gestation to 4 months of age. Delayed puberty usually occurs due to reduced estradiol levels resulting from either hypothalamic and/or pituitary dysfunction or from damage in the ovary (Pine, Hiney, Lee, & Dees, 2008).…”
Section: Discussionsupporting
confidence: 91%
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“…The VO day and occurrence of the first estrus are markers of this event (Guyton & Hall, , 1996). In the present work, both parameters were delayed in females after prenatal arsenic exposure corroborating the findings of Dávila-Esqueda et al (2012) in female rats exposed to 3 ppm sodium arsenite in drinking water from gestation to 4 months of age. Delayed puberty usually occurs due to reduced estradiol levels resulting from either hypothalamic and/or pituitary dysfunction or from damage in the ovary (Pine, Hiney, Lee, & Dees, 2008).…”
Section: Discussionsupporting
confidence: 91%
“…However, no differences were observed in serum levels of estradiol and progesterone in these females at PND 85. Dávila-Esqueda et al (2012) also showed changes in the frequency of estrous phases in female rats exposed to 3 ppm sodium arsenite from gestation to 4 months of age, without alteration in estradiol and progesterone levels after PND 30. Thus, it is possible that changes in the HPG axis occurred only during the fetal programming in females from the sodium arsenite group, compromising their puberty onset and estrous cycle, but they were re-established during adulthood maintaining the normal serum levels of progesterone and estradiol.…”
Section: Discussionmentioning
confidence: 82%
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“…In animals, arsenic induces the spermatotoxicity (Pant, Murthy, & Srivastava, ; Waalkes, Ward, Liu, & Diwan, ) by reducing the weight of testes and accessory sex organs as well as the synthesis of male reproductive hormone especially testosterone (Sarkar, Chaudhari, Chattopadhyay, & Biswas, ). Some authors also reported that arsenic may induce gonad dysfunction through declined testosterone synthesis, apoptosis and necrosis (Davila‐Esqueda et al., ; Khan, Telangb, & Malik, ; Shen et al., ). Many studies have reported that arsenic accumulates in testes, epididymis, seminal vesicle and prostate glands (Danielsson, Dencker, Lindgren, & Tjälve, ; Pant, Kumar, Murthy, & Srivastava, ).…”
Section: Introductionmentioning
confidence: 99%
“…In males, compromised testosterone production, apoptosis and necrosis seem accountable for the arsenic‐induced gonadal dysfunction (Davila‐Esqueda et al, 2012; Shen et al, 2013). Epidemiologic studies demonstrated that arsenic exposure might deteriorate sperm quality, cause erectile dysfunction and induce infertility (Hsieh et al, 2008; Meeker et al, 2010; Nie, Pei, Han, Xu, & Mu, 2006).…”
Section: Introductionmentioning
confidence: 99%