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Developmental toxicity evaluation of emodin in rats and mice.
Birth Defects Res B Dev Reprod Toxicol. 2004 Apr; 71(2):89-101.BD

Abstract

BACKGROUND

Emodin, a widely available herbal remedy, was evaluated for potential effects on pregnancy outcome.

METHODS

Emodin was administered in feed to timed-mated Sprague-Dawley (CD) rats (0, 425, 850, and 1700 ppm; gestational day [GD] 6-20), and Swiss Albino (CD-1) mice (0, 600, 2500 or 6000 ppm; GD 6-17). Ingested dose was 0, 31, 57, and approximately 80-144 mg emodin/kg/day (rats) and 0, 94, 391, and 1005 mg emodin/kg/day (mice). Timed-mated animals (23-25/group) were monitored for body weight, feed/water consumption, and clinical signs. At termination (rats: GD 20; mice: GD 17), confirmed pregnant dams (21-25/group) were evaluated for clinical signs: body, liver, kidney, and gravid uterine weights, uterine contents, and number of corpora lutea. Fetuses were weighed, sexed, and examined for external, visceral, and skeletal malformations/variations.

RESULTS

There were no maternal deaths. In rats, maternal body weight, weight gain during treatment, and corrected weight gain exhibited a decreasing trend. Maternal body weight gain during treatment was significantly reduced at the high dose. In mice, maternal body weight and weight gain was decreased at the high dose.

CONCLUSIONS

Prenatal mortality, live litter size, fetal sex ratio, and morphological development were unaffected in both rats and mice. At the high dose, rat average fetal body weight per litter was unaffected, but was significantly reduced in mice. The rat maternal lowest observed adverse effect level (LOAEL) was 1700 ppm; the no observed adverse effect level (NOAEL) was 850 ppm. The rat developmental toxicity NOAEL was > or =1700 ppm. A LOAEL was not established. In mice, the maternal toxicity LOAEL was 6000 ppm and the NOAEL was 2500 ppm. The developmental toxicity LOAEL was 6000 ppm (reduced fetal body weight) and the NOAEL was 2500 ppm.

Authors+Show Affiliations

Sciences International Inc., Alexandria, Virginia, USA. jahnke@niehs.nih.govNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15098202

Citation

Jahnke, Gloria D., et al. "Developmental Toxicity Evaluation of Emodin in Rats and Mice." Birth Defects Research. Part B, Developmental and Reproductive Toxicology, vol. 71, no. 2, 2004, pp. 89-101.
Jahnke GD, Price CJ, Marr MC, et al. Developmental toxicity evaluation of emodin in rats and mice. Birth Defects Res B Dev Reprod Toxicol. 2004;71(2):89-101.
Jahnke, G. D., Price, C. J., Marr, M. C., Myers, C. B., & George, J. D. (2004). Developmental toxicity evaluation of emodin in rats and mice. Birth Defects Research. Part B, Developmental and Reproductive Toxicology, 71(2), 89-101.
Jahnke GD, et al. Developmental Toxicity Evaluation of Emodin in Rats and Mice. Birth Defects Res B Dev Reprod Toxicol. 2004;71(2):89-101. PubMed PMID: 15098202.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Developmental toxicity evaluation of emodin in rats and mice. AU - Jahnke,Gloria D, AU - Price,Catherine J, AU - Marr,Melissa C, AU - Myers,Christina B, AU - George,Julia D, PY - 2004/4/21/pubmed PY - 2004/12/16/medline PY - 2004/4/21/entrez SP - 89 EP - 101 JF - Birth defects research. Part B, Developmental and reproductive toxicology JO - Birth Defects Res B Dev Reprod Toxicol VL - 71 IS - 2 N2 - BACKGROUND: Emodin, a widely available herbal remedy, was evaluated for potential effects on pregnancy outcome. METHODS: Emodin was administered in feed to timed-mated Sprague-Dawley (CD) rats (0, 425, 850, and 1700 ppm; gestational day [GD] 6-20), and Swiss Albino (CD-1) mice (0, 600, 2500 or 6000 ppm; GD 6-17). Ingested dose was 0, 31, 57, and approximately 80-144 mg emodin/kg/day (rats) and 0, 94, 391, and 1005 mg emodin/kg/day (mice). Timed-mated animals (23-25/group) were monitored for body weight, feed/water consumption, and clinical signs. At termination (rats: GD 20; mice: GD 17), confirmed pregnant dams (21-25/group) were evaluated for clinical signs: body, liver, kidney, and gravid uterine weights, uterine contents, and number of corpora lutea. Fetuses were weighed, sexed, and examined for external, visceral, and skeletal malformations/variations. RESULTS: There were no maternal deaths. In rats, maternal body weight, weight gain during treatment, and corrected weight gain exhibited a decreasing trend. Maternal body weight gain during treatment was significantly reduced at the high dose. In mice, maternal body weight and weight gain was decreased at the high dose. CONCLUSIONS: Prenatal mortality, live litter size, fetal sex ratio, and morphological development were unaffected in both rats and mice. At the high dose, rat average fetal body weight per litter was unaffected, but was significantly reduced in mice. The rat maternal lowest observed adverse effect level (LOAEL) was 1700 ppm; the no observed adverse effect level (NOAEL) was 850 ppm. The rat developmental toxicity NOAEL was > or =1700 ppm. A LOAEL was not established. In mice, the maternal toxicity LOAEL was 6000 ppm and the NOAEL was 2500 ppm. The developmental toxicity LOAEL was 6000 ppm (reduced fetal body weight) and the NOAEL was 2500 ppm. SN - 1542-9733 UR - https://www.unboundmedicine.com/medline/citation/15098202/Developmental_toxicity_evaluation_of_emodin_in_rats_and_mice_ L2 - https://doi.org/10.1002/bdrb.20002 DB - PRIME DP - Unbound Medicine ER -