https://ntp.niehs.nih.gov/go/ter99002abs

Abstract for TER99002

Developmental Toxicity Evaluation for Berberine Chloride Dihydrate Administered in the Feed to Swiss (CD-1) Mice on Gestational Days 6 Through 17

CASRN: 5956-60-5
Chemical Formula: C20H18NO4.Cl.2H2O
Molecular Weight: 407.848
Report Date: April 14, 2003

Abstract

The following abstract presents results of a study conducted by a contract laboratory for the National Toxicology Program. The findings may not have been peer reviewed and were not evaluated in accordance with the levels of evidence criteria established by NTP in March 2009. For more information, see the Explanation of Levels of Evidence for Developmental Toxicity. The findings and conclusions for this study should not be construed to represent the views of NTP or the U.S. Government.

Berberine is an alkaloid isolated from plants including Hydrastis canadensis L., and the Berberidaciae family, and many other plants, including the Oregon grape root. It is the major alkaloidal component of Coptis chinensis used in Chinese herbal medicine. It has also been produced synthetically. Berberine is found in tea, herbal dietary supplements, and over-the-counter health-related products. This developmental toxicity study was designed to evaluate potential maternal and developmental toxicity in time-mated mice exposed to berberine chloride dihydrate in the feed throughout the embryo/fetal period.

Female Swiss albino (CD-1) mice were dosed through ground feed (NIH-07) containing BCD (0, 3500, 5250, or 7000 ppm) on gd 6 to 17. Calculated average daily intake of BCD was 0, 569, 841, and 1155 mg/kg/day, respectively. Calculated intake of berberine chloride was 0, 450, 666, and 915 mg/kg/day. The oral route conforms to one of the expected routes of human exposure. The dose range was based on previous screening studies (NTP, 2003d,e).

In this study, timed-mated mice (25/group) were monitored in-life for clinical signs of toxicity, feed and water intake, and body weight. At necropsy (gd 17), the following determinations were made: maternal clinical condition; body, liver, and gravid uterine weights; pregnancy status; and the number of corpora lutea. In the gravid uterus, numbers of resorbed, dead, and live fetuses were recorded. Live fetuses were weighed, sexed, and examined for external, visceral, and skeletal morphological anomalies.

No maternal mortality was observed in this study. Yellow discoloration of the fur was noted in all BCD-exposed groups due to direct contact with feed containing the test chemical. There were no other remarkable clinical signs related to BCD exposure. Maternal body weights and weight gains were comparable among groups. Absolute maternal liver weight and gravid uterine weight were not affected. Relative liver weight exhibited an increasing trend, but no distinctive dose-response pattern.

During the pretreatment period, spurious differences among groups were noted for maternal relative feed consumption (g/kg/day), such that the mid- and high-dose groups consumed more feed than controls. These differences contributed to increased maternal relative feed consumption (same groups) across the gestational period as a whole. For individual measurement periods during treatment, there were no differences among groups for maternal relative feed consumption, although a significant increasing trend was noted for the treatment period as a whole. Maternal relative water consumption (g/kg/day) was comparable among groups during the pretreatment period, but was increased at ≥5250 ppm from gd 6 to 9, 9 to 12, 12 to 15, 6 to 17 and 0 to 17, but not from gd 15 to 17.

At scheduled necropsy, pregnancy was confirmed in 21-23 females/group (88-96%). Prenatal mortality (resorptions or late fetal deaths), average live litter size and percent male fetuses did not differ among groups. Average male fetal body weight/litter was not affected by BCD exposure. A decreasing trend was noted for average female fetal body weight/litter, but the 4% reduction at the high dose was not significant. There were no significant effects on incidences of malformations or variations grouped by primary classification (external, visceral, skeletal). Percent fetuses with malformations/litter showed an increasing trend (both sexes combined), but no significant effects for either sex alone. Discontinuous rib had a somewhat higher incidence in BCD-exposed groups, but the incidence was not clearly dose related. Cleft palate occurred in 0, 1, 2 and 6 fetuses in the control through high-dose groups. This pattern was not statistically significant but appeared to be biologically relevant based on a comparison with historical control data. Percent fetuses with variations/litter and percent litters with variations were increased at the mid dose (both sexes or males, but not females), but not at the high dose, due to the collective incidences of common variations, including enlarged lateral ventricles, short rib, wavy rib or rib on lumbar I.

In summary, CD-1 mice were dosed through ground feed with BCD (0, 3500, 5250, or 7000 ppm) from gd 6 to 17. Equivocal lowest observed adverse effect level for maternal and developmental toxicity were 5250 ppm (841 mg/BCD/kg/day or 666 mg berberine chloride/kg/day), and the no observed adverse effect level were 3500 ppm (569 mg BCD/kg/day or 450 mg berberine chloride/kg/day).