The sunlight-UV (SUV) inactivation of field-applied viral and other microbial insecticides has been attributed to a direct effect on DNA or generation of highly reactive radicals, or both. Therefore, it may be possible to inhibit this inactivation by use of antioxidants or oxidative enzymes. Our objective was to determine whether antioxidants and oxidative enzymes would inhibit the UV inactivation ofBaculovirus heliothis, a singly enveloped nucleopolyhedrosis virus (HzSNPV) of larvae of theHelicoverpal Heliothiscomplex. A series of blacklight fluorescent lamps, built into a temperature control cabinet, were used to simulate the ultraviolet-A and ultraviolet-B spectrum of sunlight. Three antioxidants (propyl gallate, ascorbic acid, phenylthiocarbamide) all provided some level of UV protection of polyhedral inclusion bodies (PIB) of HzSNPV. Propyl gallate, however, provided the best protection of HzSNPV (0.2 mg/ml propyl gallate gave 99% UV protection of PIB). Fifty percent UV protection with propyl gallate, ascorbic acid or phenylthiocarbamide was obtained at 0.01 mg/ml, 1.0 mg/ml, or 0.068 mg/ml, respectively. Catalase was the best of three oxidative enzymes tested. The enzyme concentration required to provide 50% UV protection of HzSNPV with either catalase, superoxide dismutase, or peroxidase was 0.4 mg/ml, 2.3 mg/ml, or 3.8 mg/ml, respectively. The increased UV stability provided by an antioxidant or oxidative enzyme supports the hypothesis that reactive radicals, generated by SUV, can cause inactivation of field-applied viral and other microbial insecticides. Although the materials we used increased persistence of HzSNPV, none could be used practically to provide UV protection of commercial microbial insecticides. Others, however, might be used as spray-tank additives, or physically bonded to PIB to provide protection against SUV.