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Disease Control and Pest Management

Toxicity of Pyroxychlor to Pythium aphanidermatum. R. W. Tillman, Former assistant professor, Department of Plant Pathology, Kansas State University, Manhattan 66506, Present address of senior author: Department of Plant Pathology and Physiology, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061; M. W. Ferguson, research assistant, Department of Plant Pathology, Kansas State University, Manhattan 66506. Phytopathology 70:441-444. Accepted for publication 9 November 1979. Copyright 1980 The American Phytopathological Society. DOI: 10.1094/Phyto-70-441.

A dosage-response curve, based upon inhibition of mycelial growth of Pythium aphanidermatum on pyroxychlor-treated potato-dextrose agar (PDA), gave ED₅₀ and ED₁₀₀ of 3 μg/ml and 9 μg/ml, respectively. In liquid medium 10 to 100 μg pyroxychlor per milliliter was equally effective in inhibiting growth of P. aphanidermatum. Mycelia exposed 24 or 96 hr to 20 μg pyroxychlor per milliliter and transferred to PDA overcame the inhibitory effect of the fungicide and grew similarly to the control. Above 50 μg pyroxychlor per milliliter recovery of P. aphanidermatum was incomplete and the fungitoxic effects increased with concentration and exposure time. After exposure for 4 hr to 50 or 100 μg pyroxychlor per milliliter or 6 hr to 20 μg pyroxychlor per milliliter, the rate of thymidine-³H incorporation into DNA was inhibited 100, 100, and 85% of the control, respectively. After 6 hr of exposure to 100 μg pyroxychlor per milliliter incorporation of uridine-³ H into RNA and l-leucine-³ H into protein of P. aphanidermatum was 49 and 51%, respectively, of the control. Exposure for 8 hr to 20, 50, or 100 μg pyroxychlor per milliliter inhibited respiration of P. aphanidermatum 8, 25, and 48%, respectively, of the control. The primary site of action by pyroxychlor appears to involve inhibition of DNA synthesis.