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EC number: 407-000-3 | CAS number: 127519-17-9 CGL 384; TINUVIN 384
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
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Specific investigations: other studies
Administrative data
Link to relevant study record(s)
Description of key information
(Ultra)-structural morphology and biochemical parameters of liver samples from treated male and female rats, as well as fetuses and whole fetuses of treated females were investigated to provide information on molecular mechanisms responsible for toxic effects of the structural analogue EC 400-830-7. The structural analogue shares the carbonic acid part that is released upon enzymatic ester cleavage. This data was presented to the EU member state Competent Authority when the volumes exceeded the threshold of 100 tons per annum and the need for further testing had to be determined.
Whole fetuses of treated dams as well as liver samples of treated dams and their fetuses of a preliminary oral teratogenicity study (Ciba-Geigy 924011) and a prenatal developmental toxicity study conducted according to OECD guideline 414 (Ciba-Geigy 924079) as well as liver samples of males treated within a one-generation reproduction toxicity study conducted according to OECD guideline 415 (Ciba-Geigy 894538) were investigated. The biochemical and (ultra)morphological investigations (Ciba-Geigy CB 92/02, Ciba-Geigy CB 92/14 and Ciba-Geigy CB 90/23 BY, respectively) identified the test item as a peroxisome proliferator in treated males, dams and the respective fetuses, the susceptibility to which is known to be a rodent specific phenomenon.
In addition, results of these studies provide a line of evidence that the increased peroxisomal metabolism generated substantial oxidative stress to tissues. The absence of fully developed or barely inducible defense mechanisms lead to the fetotoxic effects (skin discolorations, subcutaneous and skeletal muscular hemorrhages) of the test item seen in the prenatal developmental toxicity study.
Additional information
The following data on EC no. 400 -830 -7 was used for registration at the tonnage level > 100 tpa (ELINCS Level IB):
The structural analogue is a mixture of structurally related esters of 3-benzotriazol-5-tert-butyl-4-hydroxyphenyl-propionate with polyethylene glycol. 3-Benzotriazol-5-tert-butyl-4-hydroxyphenyl-propionate is considered to be the active metabolite.
Within a prenatal developmental toxicity study conducted according to OECD guideline 414 (1981) doses of 0, 1, 30 and 150 mg/kg bw/d were administered to pregnant rats by gavage (see entry in IUCLID chapter 7.8.2; Ciba-Geigy 924079). Biochemical and morphological parameters in dam and fetal liver samples as well as whole fetuses obtained from control and high dose group upon necropsy at day 15, 18 and 21 were examined (Ciba-Geigy CB 92/14).
Major treatment related findings in dams consisted of hepatic peroxisome proliferation as evidenced by electron microscopy. This was confirmed biochemically by the induction of a number of diagnostic enzyme activities such as, lauric acid 11- and 12-hydroxylase activities, catalase activities and peroxisomal fatty acid beta-oxidation. No toxicologically relevant differences in hepatic glutathione status, liver content of malondialdehyde (product of lipid peroxidation) and activities of Se-dependent and Se-independent glutathione peroxidase were seen in treated dams.
Fetal livers from treated dams showed a striking peroxisome proliferation as early as day 15 of gestation as evidenced by electron microscopy. This finding was confirmed by induced activities of peroxisomal fatty acid beta-oxidation and lauric acid 11- and 12-hydroxylation.
In contrast to the respective dams low constitutive expression and poor or lacking inducibility of the protective fetal enzyme systems of catalase and glutathione peroxidases were seen. This presumably resulted in the decreased total hepatic glutathione content and the 2-fold increased liver malondialdehyde content at day 21 of gestation. Subcutaneous and skeletal muscular hemorrhages in fetuses from treated dams after 18 and 21 days of gestation were presumed to be the result of oxidative endothelial cell lesions. The lack of glycogen accumulation in fetuses up to day 21 of gestation was suspected to be due to oxidative stress as well.
These findings are supported by biochemical and ultrastructural investigations of livers of dams and fetuses as well as whole fetuses treated in a preliminary oral teratogenicity study (Ciba-Geigy 924011, IUCLID Chapter 7.8.2). Six females/dose/time point of satellite groups were treated from day 6 (p.c.) until necropsy on day 15, 18 and 21 with 0, 50 and 100 mg/kg bw/day. Livers of dams and fetuses as well as whole fetuses were collected and processed for biochemical and ultrastructural investigations (Ciba-Geigy CB 92/02).
Biochemical investigations of a series of parameters including protein content, catalase activity, peroxisomal beta-oxidation as well as oxidized and reduced glutathione level revealed changes which were strongly indicative of the action of the test article as peroxisome proliferator. This was confirmed by the ultrastructural findings which mainly included increased number and size of peroxisomes, some of which also showing matrical plate inclusion. In fetuses this was accompanied by the absence of fully developed defense mechanism as evidenced by the low catalase activity, diminished reduced glutathione status and the absence of glycogen stores. The concomitant fetal tissue lesions are therefore most probably attributable to oxidative damage as provoked by intensified peroxisomal metabolism.
In male rats peroxisome proliferation after treatment with the test substance was also confirmed. Within a one-generation reproduction toxicity study (OECD guideline 415, Ciba-Geigy 894538, IUCLID Chapter 7.8.1) male rats received single oral gavages at dose levels of 2, 50 and 100 mg/kg bw/d for 70 days prior to and throughout the mating period (21 days) until the start of parturition of dams. Male livers were collected and processed for biochemical and ultrastructural examinations. Biochemical investigation of a series of parameters included protein content, cytochrome P450 contents, enzymatic activities (e.g. morphine and bilirubin UGT, GST, monooxygenases) and peroxisomal beta-oxidation. Changes in the biochemical parameters (e.g. about 2 and 7-fold increased lauric acid 11- and 12-hydrocylation or about 8-fold increased peroxysomal fatty acid beta-oxidation) were strongly indicative for the action of the test article as peroxisome proliferator (Ciba-Geigy CB 90/23 BY). This was confirmed by the ultrastructural findings which mainly included changes in number and size of peroxisomes with matrical plate inclusions.
Thus, the biochemical and (ultra)morphological investigations identified the test item as a peroxisome proliferator in treated males, dams and the respective fetuses, the susceptibility to which is known to be a rodent specific phenomenon.
In addition, the results of this study provide a line of evidence in support of the hypothesis that substantial oxidative stress to fetal tissues as the consequence of strongly increased peroxisomal metabolism in the absence of fully developed or barely inducible defense mechanisms lead to the fetotoxic effects (skin discolorations, subcutaneous and skeletal muscular hemorrhages) of the test item seen in the prenatal developmental toxicity study.
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