Report on the Assessment of Contact Hypersensitivity to Rifamycin-SV in BALB/c Female Mice (CAS No. 14897-39-3)
Report Date: September 2006
The following abstract presents results of a study conducted by a contract laboratory for the National Toxicology Program. The findings have not been peer reviewed and were not evaluated in accordance with the levels of evidence criteria established by NTP in March 2009. The findings and conclusions for this study should not be construed to represent the views of the NTP or the U.S. Government.
Studies were conducted to determine the potential for rifamycin to elicit a hypersensitivity response when applied dermally to female BALB/c mice. The murine model is used extensively for screening compounds that elicit chemical hypersensitivity. A panel of immune assays including, the primary irritancy assay, the local lymph node assay, and the mouse ear swelling test were used to evaluate chemical hypersensitivity to RFM (0.1-30%). The concentrations that were used in the LLNA and MEST contact hypersensitivity assays were determined by the IA. RFM treatment levels for the MEST were 3%, 10%, and 30% for sensitization phase, and 30% for challenge phase. In the LLNA, mice were also sensitized to 3%, 10%, and 30% RFM. 2,4-Dinitrofluorobenzene was used as the positive control at a concentration of 0.15% for the irritancy test and LLNA, and 0.20% for the MEST.
Although results from the IA suggest that RFM (0.1-30%) is an irritant, the ear swelling response was not sufficient to determine the minimal irritating and maximal non-irritating concentrations for the LLNA and MEST with a high enough degree of certainty. It is for this reason that the three highest doses (3-30%) were chosen as treatment levels for the LLNA and MEST. The results demonstrate that RFM is not a contact allergen to BALB/c mice. RFM did not induce cell proliferation in the draining lymph nodes and did not elicit a delayed type hypersensitivity response, as measured by the LLNA and MEST, respectively. The positive control, DNFB, induced cell proliferation in the DLN and elicited a DTH response.
The studies were conducted at the Virginia Commonwealth University Campus/Medical College of Virginia's Immunotoxicology Laboratory.