Scaleless chicken

Elsewhere in the Symposium (1 ), Dr. Knaak and colleagues examine the dermal absorption of a series of organophosphates in the rat using cholinesterase inhibition as a parameter. Here we describe a field test with a special experimental animal, the scaleless chicken. 

The ideal animal for studying organophosphates would be one without hair, fur or feathers capable of contracting delayed neurotoxicity. Such a creature is the scaleless chicken, a mutant with a defect in feather and scale development (2,3), developed and maintained by Dr. Ursula K. Abbott of the Department of Avian Sciences, University of California, Davis. (Figure 3) Its absence of feathers makes it an excellent animal for studies of dermally applied toxicants. Renden and Abbott found that the scaleless mutant was more sensitive to applications of trithion in mineral oil than were either normal chickens or another mutant "ichthyiotic", in a study of mineral oil-induced dermatitis ( ). 

Studies on the scaleless chicken are underway examining its suitability as a model for assessing toxicity of organophosphates. The first compound selected for field trials was the defoliant DEF (S,S,S-tributylphosphorotrithioate) used during the harvesting of cotton in California and Arizona in the fall (October-November) when air movements are frequently restricted by inversions. DEF has been the subject of sufficient complaints to place it on the pre-RPAR list, although there are no reports of acute or delayed neurotoxicity in humans when it and related chemicals are used according to recommendations. It both inhibits cholinesterases and causes delayed neurotoxicity in hens (3,6). 

The recently reported results of the study (8) demonstrated the feasibility of using the scaleless chicken for field research. 

Figure 4. Three scaleless chickens in a specially designed cage atop the spray rig.

Creatine Kinase Activity of Scaleless Chickens (Milliunits/ml plasma)... 

Featherless chickens treated with DEF under laboratory conditions developed delayed neurotoxicity. Three birds were pretreated with atropine sulfate (20 mg/kg s.c.) 30 minutes before they were injected with DEF (800 mg/kg s.c. technical grade, 94 purity, Mobay Chemical Co.). (A second injection of atropine sulfate was administered 2 hours after treatment with DEF.) Control hens received two injections of atropine sulfate as above. The birds were observed daily for changes in behavior, weighed and blood samples taken 2, 6, 13, and 20 days after treatment. Ataxia developed 12 days after treatment with DEF. CHE decreased to low levels as expected, in both scaleless (Figure 6) and normal birds (not shown), and, in this study, did not return to normal levels by 20 days. CK levels rose after treatment with DEF, but did not rise in the controls. Plasma CK activity also rose in birds treated with TOCP and parathion (11). 

Figure 5. Plasma CHE in scaleless chickens after field applications of DEF (CHE in nmol/min/mL DEF in In ng/cm2). Single-day exposures of groups are in Table 1, omitting birds on the sprayer (RIG). Modified from Ref. 8.

Figure 6. Plasma levels of CHE and CK in scaleless chickens given 800 mg/kg DEF and 40 mg/kg atropine, or atropine alone, and sampled on the days indicated (8). Three birds per group dark bars are for DEF-treated birds.

Figure 1. Plasma ChE activity in scaleless chickens after field applications of DEF. ChE in nmoles/min/ml DEF in In ug/cm. (Reproduced with permission from Ref. 14. Copyright 1980 Spr inger-Verlag, New York, Inc.)...

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