https://ntp.niehs.nih.gov/go/ter82095abs

Abstract for TER82095

Teratologic Evaluation of Oxytetracycline Hydrochloride in CD-1 Mice

CASRN: 2058-46-0
Chemical Formula: C22H24N2O9.ClH
Molecular Weight: 496.8975
Report Date: July 6, 1982

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.

Oxytetracycline hydrochloride, a commonly used antibiotic, was evaluated for teratogenicity following maternal exposure. Timed-pregnant CD-1 mice were dosed by oral gavage (po) on gestational days 6 through 15 with oxytetracycline hydrochloride (0, 1325, 1670 or 2100 mg/kg/day) in corn oil. These dose groups are referred to as OX-0, OX-1325, OX-1670 or OX-2100, respectively. Dams were weighed on gestational days 0, 6 through 15 (prior to daily dosing) and 17 (immediately after sacrifice) and were also observed for clinical signs of toxicity. At sacrifice on gestational day 17, dams were evaluated for body weight, liver weight, gravid uterine weight and status of uterine implantation sites (i.e., sites, resorptions, dead fetuses, live fetuses). Live fetuses were dissected from the uterus and evaluated for live litter size, body weights, sex ratios and gross morphological abnormalities. All live fetuses were examined for visceral malformations employing the Staples' fresh tissue dissection method. Half of the fetuses were decapitated prior to dissection and the heads were fixed in Bouin's solution for free-hand sectioning and examination (Wilson's technique). All fetal carcasses were stained with Alizarin Red S and examined for skeletal malformations.

The maternal mortality rate in the present study was 0.0% (0/42 dams) for the OX-0 control group, 2.4% (1/42) for the OX-1325 group, 7.1%, (3/42) for the OX-1670 group and 7.1% (3/42) for the OX-2100 group. A significant dose response trend (p less than 0.05) for reduction in maternal body weight was observed on gestational day 17, but not on gestational days 0, 6 (immediately prior to the first dose), 11 or 15 (at the completion of the dosing period). There were no significant differences, among dose groups for indices of maternal weight gain during the gestation period, during the treatment period, or in absolute weight gain. At sacrifice on gestational day 17 a dose-response trend was evident for reduction in gravid uterine weight, with the OX-2100 dose group values significantly reduced (p less than 0.01) relative to control values. Maternal liver weight was similarly reduced in the high dose group relative to controls (p less than 0.01) with a significant dose-response trend. Relative maternal liver weight values did not vary among dose groups.

Maternal weight loss of more than one gram per day was considered to be a clinical sign of toxicity in individual dams and was observed in 9.5% (4/42) of the OX-2100 dams, 2.4% (1/42) of the OX-1670 dams and in 4.8% (2/42) of the OX-1325 dams as earIy as the second day of treatment. One out of 42 dams in the OX-0 group (2.4%) exhibited weight loss in the same time period. Other clinical signs observed in a dose-response pattern included alopecia, rough coat, wheezing, hyperpnea, paresis and lethargy. Data concerning the status of uterine implantation sites exhibited a variable response. There were no statistically significant dose-related differences for the following measures: number of implantation sites per dam, number or percentage of resorptions, fetal deaths, non-live fetuses (dead plus resorbed) or affected fetuses (non-live plus malformed) per litter, or for the proportion of litters with one or more resorptions, fetal deaths, non-live, or affected fetuses. The number of litters with resorptions was significantly elevated in the OX-1325 group relative to controls but not in the two higher dose groups (OX-1670 or OX-2100). In live litters (i.e. litters with one or more live fetuses) there was no difference in the number of live fetuses per litter or in the proportion of males to females per litter across treatment groups. Body weights of live fetuses from OX-treated litters exhibited a reduction which was significant for dose-response trend (p less than 0.01) , but not for any treatment group relative to controls. When separated by sex, average male and female body weights per litter also exhibited a significant dose-response trend for reduction (p less than 0.05), although values for any treatment group were not significantly different from control values. There were no significant differences among treated and control litters in the number or percentages of males, females or live fetuses malformed nor in the number of litters with malformed fetuses. Examination of malformation incidence by category produced no evidence of dose-response trends nor evidence of any malformation unique to or with higher incidence in any of the experimental groups relative to controls.

In conclusion, no evidence for teratogenicity of oxytetracycline hydrochloride was seen in pregnant CD-1 mice when administered by oral gavage during the time of organogenesis at doses which produced little evidence of maternal toxicity (1325-2100 mg/kg/day). However, a marginal effect of oxytetracycline on fetal toxicity was detected as evidenced by the significant dose-response trend toward decreased fetal weight, with no significant differences between control and treated groups.