Castor oil, sulfated, ammonium salt

Endpoint summary

Description of key information

No biaoaccumulation potential

Key value for chemical safety assessment

Bioaccumulation potential:

no bioaccumulation potential

Absorption rate - oral (%):

45

Additional information

No data available on this substance. However, there are relevant published data on sulphates and sulphites.

Data on toxicokinetics can be extrapolated from the alkyl sulphated data: it can be expected that the absorption of sulphated fat liquor will be very high, due to their low solubilità, high log Kow, and similarità with the fatty oil derivatives basi components of human nutrition system.

 

Sulphites, which are commonly used as preservatives, are continuously formed in the body during the metabolism of sulphur-containing amino acids. Sulphite is rapidly oxidized to sulphate ion by sulphite oxidase in the liver (add references Vural Kucukatay et al, and Sun YP et al). Four rats given oral doses of sodium metabisulfite as a 0.2% solution eliminated 55% of the sulphur as sulphate in the urine within the first four hours (add reference for Bhagat & Locket 1960). A rapid and quantified elimination of sulphites as sulphate was also observed in man and dog (add reference for Rost 1933).

The ability of microrganisms to mineralize alkyl sulfates is ubiquitous in nature and most likely evolved in response to the abundance of natural sulfates. For linear alkyl sulfates which contain 6 or more carbons the process starts with enzymati hydrolysis of the ester bond, producing the corresponding alcohol and inorganic sulfate salt. The alcohol is enzymatically oxidised to aldehyde and carboxylic acid, which is further metabolized by beta-oxidation (Gilbert and Pettigrew, 1984) As a consequence the toxicological profile of sulphated castor oil can be also described with the profile of the corresponding castor oil.

 

Absorption - Oral

Alkyl sulfates

After oral administration, alkyl sulfates are well absorbed in rats, dogs and humans (Denner et al., 1969; Burke et al., 1975; Merits, 1975; Black & Howes, 1980). This was indicated byexcretion of up to 98 %of the dose administered (maximum for C12) in the urine and by comparison of excretion after oral and i.v. or i.p. application for C11 (Burke et al., 1976), C12 (Denner et al., 1969) and C18 (Burke et al., 1975) alkyl sulfates.

Alkane sulfonates

Alkane sulfonates are well absorbed in the gastrointestinal tract in rats. Absorption of the alkane sulfonates may decrease with increasing chain length. Excretion in the urine amounted to about 85 %for C12 to about 60 % for C16 (Taylor et al

Absorption -Dermal

Absorption by the percutaneous route is limited, since anionic surfactants tend to bind to the skin surface (Howes, 1975; Black & Howes, 1980).

Alkyl sulfates

Dermal penetrationof 14C-labeled C12ASO4Na in guinea pigs amountedto 0.35 %of the applied dose of 3 μmol. This value was obtained by comparison of the total amount excreted after i.p. or dermal application of the compound (Prottey & Ferguson, 1975).

Alkane sulfonates

Dermal penetrationof 14C-labeled C12ASO3Na in guinea pigs amountedto 0.2 %of the applied dose of 3 μmol. This value was obtained by comparison of the total amount excreted after i.p. or dermal application of the compound (Prottey & Ferguson, 1975). ., 1978).

 

Distribution

Alkyl sulfates

After application of 14.4 mg/kg of the erythromycin salt of C16 ASO4 to dogs or 250 mg/person to humans, radioactivity in plasma was maximal within 30 minutes to 2 hours of oral administration in both species indicating rapid absorption (Merits, 1975). The plasma concentration declined rapidly afterwards and reached 10 % of the maximum concentration after 6 hours, indicating rapid elimination.

Whole body autoradiography has been performed to follow the distribution of 35S-C10ASO4K (Burke et al., 1975), C12ASO4 K (Denner et al., 1969) and C18ASO4K (Burke et al., 1975) or their metabolites within the body with time in experiments with rats after i.p. injection. For all compounds the only organs, where radioactivity was detected, were the liver and the kidney (Burke et al., 1975, 1976; Denner et al., 1969). The levels (not quantified) were highest 1 h after application. C10 AS was cleared from tissues more rapidly than C18. After 6 hours, only traces of the C10 salt remained in the kidney, whereas it took 12 hours for the C18 salt to be cleared from the kidney (Burke et al., 1975; 1976).

 

Alkane sulfonates

The distribution of 35S-C12ASO3Na and 35S-C16ASO3Na has been studied in rats after dosing via gavage and i.p. administration by whole body autoradiography (Taylor et al., 1978). Accumulation of radioactivity after oral application was observed in liver and kidneys within 1 hour, but no general body distribution of radioactivity was observed with 35S-C12ASO3Na. In contrast, after application of 35S-C16ASO3Na up to 2 hours after administration the radioactivity was mainly retained in the stomach and the gastrointestinal tract. Some cellular accumulation in the liver and kidneys was detected after 30 minutes. After i.p. application peak radioactivity in liver and kidneys were already observed after 15 to 30 minutes for both compounds.

Metabolism

Alkyl sulfates

Alkyl sulfates are extensively metabolized in rats, dogs and humans. This was tested with radiolabelled C10, C11, C12, C16 and C18 alkyl sulfates, potassium salts (Denner et al., 1969; Burke et al., 1975, 1976; Merits 1975; Greb & Wingen, 1980).

The postulated mechanism is degradation involving ω-oxidation, followed by β-oxidation, to yield metabolites with chain lengths of C2 and C4 for even-chain carbon alkyl sulfates (Greb & Wingen, 1980). The major metabolite for even-chained alkyl sulfates was identified as the 4-carbon compound, butyric acid 4-sulfate. The 4-butyrolactone has been found as a minor metabolite which is also formed after application of butyric acid 4-sulfate (Ottery et al., 1970). Dog and human urine also contained one other minor metabolite, glycolic acid sulfate (Merits, 1975).

 

Alkane sulfonates

The metabolism of alkyl sulfates and alkane sulfonates is similar.

The biotransformation of alkane sulfonates (C12 and C16 have specifically been studied) also is assumed to involve ω-oxidation and β-oxidation. The major metabolite of the C12 and C16 is the analogous sulfonate butyric acid 4-sulfonate (Taylor et al., 1978; Black & Howes, 1980). However, in contrast to the alkyl sulfates no desulfonation of the molecule takes place.Table 3-4 compares the metabolism and elimination of a C12-alkane sulfonate with a C12-alkyl sulfate.

The excretion is mainly via the urine. The percentage in the feces (4.7 – 7.7 %) for the alkane sulfonate was somewhat higher than for the corresponding alkyl sulfate. In addition to the C12 compound also a C16 compound has been investigated (Taylor et al., 1978). Only the parent compound could be found in the feces which amounted to 37.1 - 46.4 % of the dose (2 male and female rats). Biliary secretion was less than 1 % of the dose. Therefore this reflects unresorbed compound.