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EC number: 204-815-4
CAS number: 126-97-6
Read-across from supporting substance (structural analogue or surrogate): In 13-week dermal subchronic toxicity studies in rats and mice with sodium thioglycolate, no treatment-related effects on sperm density and motility, caudal epididymal sperm, spermatid head counts in the testes and testis weights, as well as oestrous cycles, were observed up to dose levels of 180 and 360 mg/kg bw/d, respectively.
Study (OECD 416)
effects of NaTG on the integrity and performance of the male and female
reproductive systems, including gonadal function, the estrous cycle,
mating behavior, conception, gestation, parturition, lactation and
weaning, and on the growth and development of the offspring was
evaluated over 2 generations (Davies, OECD 416).
groups of 25 male and 25 female Sprague-Dawley rats received NaTG daily
for 10 weeks prior to mating, during mating, gestation and lactation
until weaning of the pups. NaTG was administered by oral gavage at
dose-levels of 10, 20 or 40 mg/kg/day. Another group of 25 males and 25
females received the vehicle alone under the same experimental
conditions and acted as a control group. A constant dosage volume of 5
mL/kg/day was used. The animals were checked at least twice daily for
mortality or morbidity and at least once daily for clinical signs. A
detailed clinical examination was performed once before the beginning of
the treatment period and then once a week. Body weight and food
consumption were recorded weekly. The estrous cycles were monitored
during the last 3 weeks before mating and during the mating period,
which lasted up to 13 days. The females were allowed to litter and rear
their progeny until weaning. The pups were regularly weighed throughout
the lactation period and observed daily for clinical signs. Physical and
reflex development was assessed (pinna unfolding, hair growth, tooth
eruption, auditory canal opening, eye opening, surface righting, cliff
avoidance and air righting). At the end of the treatment period or prior
to premature sacrifice, the F0 animals were blood sampled for analysis
of hematology and blood biochemistry parameters, including
ß‑hydroxybutyrate and acetoacetate determination. The animals were not
fasted before blood collection. After weaning of the pups, the males and
females of the F0 generation were sacrificed. Sperm analysis was
performed on the first 10 males of the control and high-dose groups
(groups 1 and 4) and since no treatment-related effects were observed
this was not performed on males of the other groups. A complete
macroscopic examination was performed, including counting the number of
implantation sites in females, and designated organs were weighed. A
microscopic examination was performed on the reproductive organs and
macroscopic lesions of all groups and for the control and high-dose
groups the heart, kidneys and liver were also examined. The liver of all
intermediate-dose group animals was also examined. Of the progeny of the
F0 generation, one or two males and one or two females per litter were
selected to constitute the F1 generation of groups of 25 male and 25
female rats in the control, low and intermediate groups and 27 male and
27 female rats in the high-dose group (this to compensate in advance for
mortality around the time of delivery, a known effect of the test item).
Three groups received NaTG daily for 10 weeks prior to mating, during
mating, gestation and lactation until weaning of the pups. Due to the
test item inducing known difficulties around the time of delivery, all
mated females, including controls, were not treated from day 19 of
gestation until day 1 of lactation in order to see if this would reduce
the mortality. The test item was administered by oral gavage at dose
levels of 10, 20 or 40 mg/kg/day. Another group of 25 males and 25
females received the vehicle alone under the same experimental
conditions and acted as a control group. A constant dosage volume of 5
mL/kg/day was used. The animals were checked at least twice daily for
mortality or morbidity and at least once daily for clinical signs. A
detailed clinical examination was performed once at weaning before the
beginning of the treatment period and then once a week. Body weight and
food consumption were recorded weekly. Each animal was assessed for
sexual maturity (balanopreputial separation or vaginal opening) and the
day of age and body weight was recorded on the day each animal was
positive. At 4 weeks of age, the animals were assessed for auditory
function (acoustic startle response) and pupil constriction, and weeks
of age the spontaneous locomotor activity was measured using automated
infra-red sensor equipment. The estrous cycles were monitored during the
last 3 weeks before mating and during the mating period, which lasted up
to 19 days. The females were allowed to litter and rear their progeny
until weaning. The pups were regularly weighed throughout the lactation
period and observed daily for clinical signs. Physical and reflex
development was assessed (pinna unfolding, hair growth, tooth eruption,
auditory canal opening, eye opening, surface righting, cliff avoidance
and air righting). In addition, the anogenital distance of all pups was
measured on the day after birth and the presence of nipples was checked
in all males on post-natal day 12 or 13. At weaning of the pups, the
males and females of the F1 generation were sacrificed. Sperm analysis
was performed on the first ten males of the control and high-dose groups
(groups 1 and 4). A complete macroscopic examination was performed,
including counting the number of implantation sites in females, and
designated organs were weighed. A microscopic examination was performed
on the reproductive organs and any macroscopic lesions of all groups. In
addition, pups of both the F0 and F1 animals were submitted for a
macroscopic examination. One randomly selected pup/sex/litter for F1 and
F2 litters, all pups found dead or prematurely sacrificed and any pups
showing external abnormalities or clinical signs were weighed and then
submitted for a macroscopic examination of the principal thoracic and
abdominal organs with special attention paid to the reproductive organs.
were no effects of treatment at 10 or 20 mg/kg/day.
40 mg/kg/day, the males and females showed no effects of treatment
during the pre-mating, mating or gestation phases. At delivery, four
females were found dead; one on gestation day 21 and three on gestation
day 22. One of these females found dead on gestation day 22 had
delivered 12 live and one dead pup before dying; the other three females
had not started delivery and had dead fetuses in the uterine horns at
necropsy. On lactation day 1, one female, showing signs of poor
condition (piloerection, blood and placentae in the bedding),
cannibalized her 10 pups (it is likely that more pups were born and
cannibalized before being noticed because there were five more
implantation sites in the uterine horns than pups). It is not known
whether the pups were alive or dead prior to cannibalism, however the
adverse outcome is considered to be a maternal effect since no fetuses
remained in the uterine horns at necropsy; the female did deliver all
pups starting delivery on gestation day 21. No effects of treatment were
observed in the F0 generation animals during the remainder of the
lactation period other than a slightly lower mean body weight gain of
the females during the first 4 days of lactation. There were no effects
on sperm parameters in the control or high-dose group males. There were
no treatment-related effects on organ weights at any dose-level. There
were no treatment-related microscopic changes in testis, epididymis,
prostate, coagulating glands or seminal vesicles. There were possible
treatment-related changes in the uterus of one 40 mg/kg/day female (one
female which had only implantation scars thought to be left from early
resorptions); thrombosis of the mesometrial remnant, organized by
granulation tissue composed of fibroplasia, fibrin plugs, thrombi and
neovascularization. Golden pigment-laden cells and pyknotic
trophoblastic cells were observed. Female had hemorrhage of a
mesometrial triangle. Minimal to moderate periportal hepatocellular
microvacuolation was observed at 40 mg/kg/day in 2/25 males and 6/25
females, and in 4/6 prematurely sacrificed/found dead females suggesting
mild liver toxicity at this dose-level. No control animals had the same
plasma fatty acid concentration was statistically significantly
decreased however there were no effects of treatment with the test item
on plasma acetoacetate or ß-hydroxybutyrate concentrations indicating
that the animals were not in ketosis.
were no effects of treatment on F1 pups in the 10 or 20 mg/kg/day groups.
40 mg/kg/day, the pups had a 9.6% mortality rate during the first 4 days
of lactation (cannibalism and being found dead); neither the pups nor
the F0 dams showed particular clinical signs (except one female which
had piloerection and cannibalized all pups in the litter). There was a
possible, very slight, delay in physical development; the majority of
the pups achieved tooth eruption, eye opening and auditory canal opening
on the same day as the majority of the pups from the other groups but
there was a higher percentage of pups achieving these landmarks on later
days than in the other groups. The females of the F1 generation started
treatment (on day 22 of age) with a statistically significantly lower
mean body weight than the controls. Mean body weight gain and mean food
consumption were both also statistically significantly lower for the
first week of treatment. During gestation, the females had a slightly
lower body weight gain. Treatment was stopped on gestation day 19 and
delivery passed without problem in all females. However, two females
were prematurely sacrificed on day 2 or day 5 of lactation due to death
of the litter. One of the females had thrombosis of mesometrial
triangles. Treatment was re-started on lactation day 1 and the number of
pup deaths was higher when compared with the controls. This was mainly
due to one female which had three found dead pups and cannibalized 13
pups over several days until lactation day 5 when all pups were dead.
Another female also had total litter death but delivered only one pup.
The total number of dead pups in this group was similar to that of the
controls when the female with the 16 dead pups is excluded (15 dead pupsvs.control
group), but whereas the control pup deaths were concentrated in four
litters, at 40 mg/kg/day the pup deaths were spread over seven litters.
The females had not had any noticeable problems during delivery and were
not showing any clinical signs during the first days of lactation except
for a possible effect on maternal nesting and nursing behavior since the
pups were often observed to be cold, even those that survived. There
were no treatment-related effects on organ weights at any dose-level.
There were no effects on sperm parameters in the control or high-dose
group males. There were no treatment-related microscopic changes neither
in testis, epididymis, prostate, coagulating glands or seminal vesicles
of the males nor in the ovaries, oviducts, uterus and vagina of the 40
mg/kg/day of the females.
female F2 pups had a slightly lower mean body weight at the end of
lactation (-5%) but there were no effects on male or female F2 pup
physical development in terms of eye opening, tooth eruption or auditory
canal opening or on reflex development.
40 mg/kg/day, it is concluded that the test item has no effect on
non-pregnant, naïve, adult rats but that it causes maternal toxicity and
death of susceptible pregnant females around the time of delivery.
Effects on the dam include lack of nesting/nursing behavior and this
causes death of the pups which have been delivered. If treatment is
stopped just prior to delivery, the females may survive delivery but pup
death may still occur and pup clinical signs of coldness suggest that
maternal nesting/nursing behavior is still impaired by treatment with
the test item and affect pup survival. There is evidence that female
rats are more affected by test item treatment than males as shown by
lower F1 female body weight and body weight gain.
to moderate periportal heptocellular microvacuolation was observed in
females and some male F0 animals treated at 40 mg/kg/day suggestive of
mild hepatotoxicity and especially in dams (4/6) found dead or
prematurely sacrificed at time of parturition. NaTG is known to induce
fatty liver via an inhibition of theβ-oxidation
of fatty acids.
were no effects on sperm parameters in the control or high-dose group
were no effects of treatment on any parameters measured in either males
or females with the test item at 10 or 20 mg/kg/day.
the experimental conditions of this study, and in view of the maternal
mortalities and liver effects in males and females observed at 40
mg/kg/day, the dose-level of 20 mg/kg/day was considered to be the No
Observed Effect Level (NOEL) for parental toxicity, female fertility and
gestation of each generation and for development, growth and survival of
the progeny. It is probable that the small effects observed on pup
survival at 40 mg/kg/day was secondary to the severe and lethal effects
observed in the pregnant dams at that dose level. The No Observed Effect
Level (NOEL) for males fertility and female mating behavior was higher
or equal than 40 mg/kg/day.
Screening Study (OECD 421)
a reproduction/developmental screening test performed according to the
OECD Guideline 421, four groups of 12 male and 12 female Sprague-Dawley
rats received sodium thioglycolate (purity 98.9% pure), daily, by oral
(gavage) administration, 10 weeks before mating and through mating and,
for the females, through gestation until day 5 post-partum at
dose-levels of 0, 20, 40 or 80 mg/kg bw/d.
signs and mortality were checked daily. Body weight and food consumption
were recorded weekly until mating and then at designated intervals
throughout gestation and lactation. The animals were paired for mating
and the dams were allowed to litter and rear their progeny until day 5 post-partum.
The total litter sizes and numbers of pups of each sex were recorded
after birth, pup clinical signs were recorded daily and pup body weights
were recorded on days 1 and 5 post-partum. The males were
sacrificed after completion of the mating period and the females on day
5 post-partum (or on day 25 post-coitum for females which
did not deliver). The body weight and selected organs (brain,
epididymides, heart, kidneys, liver, ovaries, prostate, seminal vesicles
and testes and uterus) were weighed and a macroscopic post-mortem examination
of the principal thoracic and abdominal organs and a microscopic
examination of selected organs (macroscopic lesions, epididymides,
heart, kidneys, liver, ovaries, prostate, seminal vesicles, testes, and
uterus) were performed. In the females, which were apparently
non-pregnant, the presence of implantation scars on the uterus was
checked using ammonium sulphide staining technique. Epididymal sperm was
sampled for motility, morphology and count and testicular sperm heads
resistant to homogenization (i.e. elongated spermatids and mature
spermatozoa) were counted. The pups were sacrificed on day 5 post-partum
and were carefully examined for gross external abnormalities and a
macroscopic post-mortem examination was performed.
males and one female given 80 mg/kg bw/d were found dead during the
pre-mating or mating periods with no clinical signs observed before
death and no relevant post-mortem findings. Four females at 80
mg/kg/d and one at 40 mg/kg bw/d were found dead or were prematurely
sacrificed because of difficulties to deliver. Ptyalism was observed at
40 and 80 mg/kg bw/d with a dose-related incidence and may be related to
the taste of dosing solution. All male and female groups had body weight
gains comparable with the controls throughout the study. There were no
adverse effects of treatment on mean food consumption, except a slight
lowering of food consumption during the lactation period for females
given 80 mg/kg bw/d.
mean number of estrous cycles in each group was between 4 and 5 during
the period measured and the mean cycle length was a normal 4 or 5 days.
All pairs mated and the majority of the females were pregnant. There
were no effects of treatment on the mean number of days taken to mate.
given 80 mg/kg bw/d had a statistically significantly longer gestation
period, a non-statistically significantly lower number of corpora
lutea and a statistically significantly lower number of
implantations and pups. One female had total resorptions and one litter
died on day 1 post-partum.
were no effects of treatment on sperm morphology, motility or counts.
The mean absolute seminal vesicle weights were statistically
significantly lower for all treated groups compared to the control
group, but the mean relative weight was only decreased at 80 mg/kg bw/d.
For all treated groups, the absolute weights were in the range of the
historical control data. Only at 80 mg/kg bw/d, the relative weight was
outside the historical data and was correlated with a slight decrease in
secretory content in the seminal vesicles. There were no
treatment-related adverse effects in pups based on clinical signs, mean
body weight gain and necropsy findings.
NOAEL for parental toxicity was considered to be 20 mg/kg bw/d (based on
deaths at 40 and 80 mg/kg bw/d), the NOAEL for reproductive performance
(mating, fertility and delivery) was considered to be 20 mg/kg bw/d
(based on deaths at 40 and 80 mg/kg bw/d) and the NOAEL for toxic
effects on progeny was 40 mg/kg bw/d (based on the dead litter at 80
mg/kg bw/d which cannot definitively be attributed to maternal
Short description of key
Thioglycolic acid and its salts are not considered to be
reproductive toxicants. The conducted reproduction toxicity studies with
sodium thioglycolate can be bridged to other salts of the thioglycolic
acid, because in aquous solutions only the organic thioglycolate anion
may have the potential to cause reproduction toxicity.
The developmental toxicity of ammonium and sodium thioglycolates has been investigated in standard oral and dermal studies in rats and/or rabbits compliant or comparable to OECD guideline 414, respectively.When ammonium thioglycolate was administered by gavage, the NOAELs for maternal and embryo-foetal toxicity were 15 and 75 mg/kg bw/d, respectively. No teratogenic effects were observed in all studies.In the dermal studies with sodium thioglycolate, the NOAELs for maternal toxicity was < 50 mg/kg bw/d in Sprague-Dawley rats and > 65 mg/kg bw/d in New Zealand White rabbits. The developmental toxicity NOAEL was 100 mg/kg bw/d and >65 mg/kg bw/d, respectively.
developmental toxicity potential of ammonium thioglycolate by the oral
route was evaluated in rats in a study performed according to the OECD
Guideline 414 (Gleich, 1998).
thioglycolate was administered by gavage to 3 groups of 25 pregnant
Wistar rats from gestation days (GD) 6 to 19 at daily doses of 0, 3, 15,
and 75 mg/kg bw/d.
Day 0 of pregnancy was designated as the day of confirmed mating.
Clinical signs including mortality and evidence of abortion were checked
daily. Body weight was determined on GD0, 6 and then daily until GD20.
Food and water consumption was recorded at designated intervals during
pregnancy. On day 20 of pregnancy, females were killed. The terminal
body weights of the dams were recorded. The gravid uterus was weighed
and foetuses removed by hysterectomy. Females were examined
macroscopically. Litter parameters were recorded: number of corpora
lutea, implantation sites, early and late resorptions, and dead and live
foetuses. Foetuses were weighed, sexed, and submitted to external
examination. About half of them were examined for skeletal malformations
and half for organ malformations.
the bedding material was seen in all rats in the high dose group. Two
animals in the high dose group died on GD 20, one day after the last
administration of the test material. These deaths were regarded to be
treatment related. Eighteen to 24 rats out of 25 per group proved to be
pregnant. The body weight development, food and water consumption were
not affected by treatment. The terminal body weights were similar in all
groups. The uterus weights in the high dose group were slightly, but not
significantly lower than in the control or the other groups. This
finding was regarded to be accidental. The numbers of corpora lutea,
implantations and live foetuses were not affected. The numbers of dead
foetuses, and complete, early and late resorptions were not increased.
The sex distribution was not affected in any of the groups. The weights
of the foetuses in the low, mid, and high dose groups were similar to
the control and not affected by treatment. The frequency of all
malformations was in a normal range and not increased. The NOAELs for
maternal and embryo-foetal toxicity were 15 and 75 mg/kg bw/d,
respectively. No teratogenic effects were observed.
developmental toxicity of sodium thioglycolate by the dermal route was
evaluated in pregnant rats and rabbits in studies performed according to
a method comparable to the OECD guideline 414 (Tyl, 2001a,b; Tylet al.,
Sprague-Dawley rats or New Zealand White Rabbits were exposed topically, 6
hr/day, to sodium thioglycolate
(99% pure) in vehicle (95% ethanol:distilled water, 1:1) from
gestational day (GD) 6 through 19 at dose levels of 0, 50, 100, and 200
mg/kg bw/d for rats orfrom GD 6–29
at 0, 10, 15, 25 or 65 mg/kg bw/d
timed-mated female rats or twenty-four naturally mated female rabbits
(in two replicates of 12) were assigned to each group and monitored at
regular intervals throughout gestation for clinical signs (including
dosing site condition), feed and water intake, and body weight. At
necropsy on gestational day 20 or 30, respectively; the following were
recorded: maternal clinical condition; body, liver, kidney (rabbits
only) and gravid uterine weights; and pregnancy status. The number of
ovarian corpora lutea and uterine implantations (resorbed, dead, or live
foetuses) was recorded. All live foetuses were counted, weighed, and
examined for external alterations, including cleft palate. Approximately
50% of the live rat foetuses or 100% of the live rabbit foetuses per
litter were sexed internally and examined for visceral alterations.
These foetuses were decapitated and the heads fixed, decalcified, and
examined for soft tissue craniofacial alterations. All foetal carcasses
were eviscerated (and rat foetuses not scheduled for a visceral
examination were sexed internally), macerated, and stained with alizarin
red S and alcian blue. Intact rat foetuses (those not decapitated) and
all rabbit foetuses were examined for ossified and cartilaginous
sodium thioglycolate treatment was associated with one maternal death at
200 mg/kg/d (only clinical observations at the dosing site preceded
death). Other effects, dependent on dose and exposure duration, included
body weight and weight gain reductions, changes in relative feed and
water intake, and discoloration and slight erythema at the application
site. Feed consumption was significantly increased above the control at
50 and 100 mg/kg bw/d, but not at 200 mg/kg bw/d. Maternal water
consumption was significantly increased at 200 mg/kg bw/d and slightly
(but not statistically significantly) increased at 50 and 100 mg/kg
bw/d. Maternal body weights and body weight changes were decreased only
at 200 mg/kg bw/d.
scheduled necropsy, there were no macroscopic indications of organ
toxicity. In addition, organ weights and gravid uterine weights were
equivalent across groups; maternal body weight was significantly reduced
at 200 mg/kg/d. Prenatal viability was unaffected by maternal exposure
to sodium thioglycolate. The incidences of foetal external, visceral,
and skeletal alterations were also unaffected. A significant,
dose-related, upward trend was present for % foetuses with skeletal
variations per litter, but there were no significant pairwise
comparisons to the vehicle control group value and the % were in the
range of the historical control data. Body weights of male and female
foetuses per litter at 200 mg/kg bw/d were significantly lower than
maternal NOAEL could not be identified (<50 mg/kg bw/d), while the
developmental toxicity NOAEL was 100 mg/kg bw/d.
no maternal deaths were associated with sodium thioglycolate treatment.
One female in the 25 mg/kg bw/d group delivered early and one doe in the
65 mg/kg bw/d group was removed due to a preexisting condition
(trichobezoar or hairball in the stomach). Clinical observations were
almost exclusively limited to effects of treatmentat
the dosing site (skin erythema) in all groups.
body weight and body weight gain were equivalent across dose groups for
all intervals measured except for body weight gain for gestational days
12-15. There was a trend for decreased body weight gain for this
interval, which was significant in the high dose group when compared to
controls. There were no consistent treatment related reductions in feed
consumption.At scheduled necropsy, there was no effect of treatment on
terminal maternal body weight. In addition, organ weights and gravid
uterine weights were equivalent across groups.
viability was unaffected by maternal exposure to sodium thioglycolate.
The incidences of foetal external, visceral, and skeletal alterations
were also unaffected. Body weights of male and female foetuses per
litter and percent males and females per litter were equivalent across
maternal NOAEL for systemic toxicity was at or above 65 mg/kg bw/d; for
local toxicity at the dosing site, it was below 10 mg/kg bw/d. The NOAEL
for developmental toxicity was >65 mg/kg bw/d.
the end of a sub-chronic (90-day) toxicity studies of sodium
thioglycolate administered by cutaneous application to F344/N rats and B6C3F1 mice,
a special sperm morphology and vaginal cytology evaluation (SMVCE) was
performed (Wolfe and Seung, 2003a,b).
density and motility, caudal epididymal sperm, spermatid head counts in
the testes and testis weights, as well as of vaginal cytology, to allow
examination of oestrous cycles, were examined in rats and mice for the
controls and three top dose groups.
differences were observed between the control and treated groups in the
female oestrous cycles, in length of cycle, stages, number of females
cycling and number of females with regular cycles in either rats or
mice. No differences were observed between controls and treated males in
sperm parameters or in testicular spermatid counts, or testes and
epididymal weights in either rats or mice. However, in mice, the number
of sperm per mg cauda, and per total cauda were decreased at 180 and 360
mg/kg bw/d but the reduction was not statistically significant. As the
histopathological examination of the testes and epididymis (of rats and
mice) performed in these 90-day studies did not show any evidence of
damage, this non-significant difference in sperm numbers observed in
mice can be dismissed as an incidental finding.
mercaptoacetic acid and its salts are not considered to be developmental
or reproductive toxicants, except at dose levels associated with
mortality was observed in the OECD 421 and OECD 416 studies in rats at
doses of 40 and 80 mg/kg bw/day. The acute oral LD50 of sodium
mercaptoacetate (NaTG) is 50 – 200 mg/kg bw in fasted animals and the
lethal doses in the reproductive toxicity studies fall into this range.
the mortalities of pregnant dams cannot be regarded as reproductive
toxicity, but rather a direct consequence of the established toxic mode
of action of mercaptoacetates. Mercaptoacetates are known inhibitors of
mitochondrial fatty acid β-oxidation. Studies with NaTG have shown that
hypoglycaemia occurs in rats dosed with NaTG via oral gavage and that
this effect is pronounced in fasted compared to non-fasted animals
(Grosdidier 2011, Report No. 37043, IUCLID Section 7.9.4). The
hypoglycaemia is a result of impaired gluconeogenesis secondary to
inhibition of fatty acid catabolism by mercaptoacetate. Ad-libitum
feeding, as employed in the OECD 421 and OECD 416 studies, apparently
saves the animals from succumbing already after a single gavage dose by
providing a sufficient external glucose supply. Maternal death in NaTG
treated dams occurred in late pregnancy (GD 21-23) or early after
parturition (PND 1-2). It is likely that the enhanced energy demand due
to parturition and / or lactation further exhausts the glucose reserve
of the dams ultimately contributing to their death.
classification as toxic to reproduction is not justified since all
maternal and foetal/offspring effects are directly related to the
observations leading to a classification as Acute Tox 3 – H301: Toxic if
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