Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 231-901-9
CAS number: 7778-39-4
A review article was published by Wang
et al. (2006) describing the reproductive and developmental effects of
arsenic and analogues.
Male reproductive toxicity:
Arsenite given through drinking water or by
i.p. injection interferes spermatogenesis and lowers levels of
testosterone and gonadotrophin causes male reproductive toxicity; these
results suggest that arsenic may act on the brain or pituitary as well
as directly on the germ cells (Chinoy et al., 2004; Pant et al., 2001,
2004; Sarkar et al., 2003).
- Male mice exposed to sodium arsenite in
drinking water at up to 533.90μmol/L for 35 days
showed reproductive toxicity without clinical effects. AsIII-treated
mice did not show changes in body weight, testes weight, or accessory
sex organ weights. However, at 533.90μmol/L, the
activity of 17β-hydroxysteroid dehydrogenase (HSD) was
decreased and conversely, the activities of lactate dehydrogenase (LDH)
andγ-glutamyltranspeptidase (γGT) were increased
in the testes. LDH was used as a marker of Leydig cell function, andγGT
as a marker of Sertoli cell function. AsIII-treated mice also showed
decreases in sperm count and motility along with an increase in abnormal
sperm (Pant et al., 2001).
- Swiss albino mice were given sodium
arsenite at 53.39μmole/L (equivalent to 4 ppm
arsenic) via drinking water for 365 days, causes decreased testicular
weights, sperm count and sperm motility and the percentage of abnormal
sperm was increased. It also affects the activities of marker testicular
enzymes which ultimately causes damage to germ cells (Pant et al.,
- Sodium arsenite was administered to Wistar
rats via i.p. injections at 4, 5, or 6 mg/kg/day for 26 days. At 5 and 6
mg/kg/day, relative testicular weight, accessory sex organ weights and
epididymal sperm counts were decreased. Arsenic induced low levels of LH
and FSH might be the trigger of suppressed testosterone synthesis, leads
to increased spermatid degeneration (Sarkar et al., 2003).
Male Swiss mice were administered with arsenic trioxide orally at 0.5
mg/kg for 30 days, affects the spermatogenesis, cholesterol metabolism
and testicular testosterone level. Co-exposures to arsenic and fluoride
(NaF) found that the recovery from arsenic and fluoride-induced effects
can be facilitated by ascorbic acid, calcium, and vitamin E, which
suggests that arsenic and fluoride induced reproductive toxicity was at
least in part mediated by oxidative stress (Chinoy et al., 2004).
Female reproductive toxicity:
In female mice and rats, inorganic arsenic
suppresses ovarian steroidogenesis, prolongs diestrus, and degenerates
ovarian follicular and uterine cells. It also increases meiotic
aberrations in oocytes, and decreases cleavage and pre implantation
development (Chattopadhyay et al., 2001; Navarro et al., 2004; Zhang et
- Female Wistar rats gavaged with 10 mL of
0.4 ppm sodium arsenite daily for 28 days, causes uterine and ovarian
toxicity, prolonged diestrous (due to low estradiol), decreased relative
ovarian and uterine weights and affects the neuroendocrine regulation of
female sex hormones (decreased LH, FSH, and estradiol). Decreased FSH
level may contribute to the degeneration of ovarian follicles. It also
causes uterine cell degeneration may be due to low ovarian estradiol
and/or increased production of reactive oxygen species after arsenic
treatment. The primary cause of AsIIItoxicity in the female
reproductive system could be arsenic induced changes in the levels of
catecholamines in the brain, which lowers gonadotrophin synthesis and
secretion (Chattopadhyay et al., 2001, 2003).
- Female CD-1 mice were injected with 0, 8,
or 16 mg/kg sodium arsenite i.p. every 2 days for a total of 7
injections over 14 days followed by injections of equine and human
chorionic gonadotrophins overlapping the end of AsIII treatment
to induce superovulation. AsIII induces oocyte meiotic aberrations and
could subsequently decrease oocyte fertilization, preimplantation
development, and embryo viability. Some of these arsenic effects on
oocytes were observed at 8 mg/kg, which was a previously established
maternal no-observed-adverse-effect level (NOAEL) (Navarro et al., 2004).
A review article was published by Wang et
al. (2006) describing the reproductive and developmental effects of
arsenic and analogues. Exposure to inorganic arsenic and analogues
through drinking water or by i.p. injection causes male reproductive
toxicity by interfering spermatogenesis and lowering levels of
testosterone and gonadotrophin. This suggested that arsenic may act on
the brain or pituitary as well as directly on the germ cells. (Chinoy et
al., 2004; Pant et al., 2001, 2004; Sarkar et al., 2003). In
female mice and rats, inorganic arsenic suppresses ovarian
steroidogenesis, prolongs diestrus, and degenerates ovarian follicular
and uterine cells. It also increases meiotic aberrations in oocytes, and
decreases cleavage and pre implantation development (Chattopadhyay et
al., 2001; Navarro et al., 2004; Zhang et al., 2000).
In conclusion, exposure to inorganic arsenic
and analogues via oral or intraperitoneal route has shown adverse
effects on reproduction in mice and rats.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
Damit Sie die Website optimal nutzen können, verwenden wir Cookies.
Welcome to the ECHA website. This site is not fully supported in Internet Explorer 7 (and earlier versions). Please upgrade your Internet Explorer to a newer version.
Do not show this message again