The toxicity of Kaempferia galanga rhizome-derived methanol extract (RME), powder (RP) and steam distillate (RSD) to Meloidogyne incognita second-stage juveniles (J2) and eggs, and their effects on Lycopersicon esculentum germination and growth were examined in vitro and in pot experiments. Results were compared with those of three nematicides: carbofuran, fosthiazate and metam sodium. In contact + fumigant bioassays with J2, RME applied at 1, 0.5 and 0.25 mg (g soil) −1 resulted in 92, 88 and 73% mortality, respectively. The lethality of RME was almost the same as carbofuran but lower than that of either fosthiazate or metam sodium. RSD and RP were less active than RME. In vapour-phase mortality bioassays with J2, the test materials were more effective in a closed container than in an open one, indicating that mode of delivery was, in part, a result of vapour action. In direct-contact mortality bioassays with M. incognita eggs, RME, RSD and fosthiazate treatments resulted in 91, 100 and 95% inhibition of hatch at 250 μg ml −1 and 82, 88 and 81% inhibition of hatch at 100 μg ml −1 , respectively. In filter paper bioassays with L. esculentum seed, 8.8 μg cm −2 RME and RP did not cause germination inhibition, while RSD and fosthiazate treatments resulted in 84 and 13% germination inhibition. In pot tests, RME and RSD applied at 8 mg (g soil) −1 reduced galling caused by M. incognita significantly, and fosthiazate at 0.02 mg (g soil) −1 stopped galling completely. Kaempferia galanga rhizome-derived materials, particularly a methanol extract, merit further study as potential nematicides and hatching inhibitors for the control of M. incognita as fumigants with contact action.
The toxicity of Kaempferia galanga rhizome constituents to second-stage juveniles (J2) and eggs of Meloidogyne incognita was examined in vitro and in container experiments. Results were compared with those of three nematicides: carbofuran, fosthiazate and metam sodium. Ethyl cinnamate (EC) and ethyl p-methoxycinnamate (EMC) were the nematicidal and hatch inhibitory principles. In direct-contact mortality bioassays, EC (0.037 mg ml −1 ) and EMC (0.041 mg ml −1 ) were more toxic than carbofuran (0.092 mg ml −1 ) but less toxic than fosthiazate (0.002 mg ml −1 ) towards J2 based upon 48 h LC 50 values. EC and EMC treatments resulted in 100% and 93 and 81% inhibition of hatch at 125.0 and 62.5 μg ml −1 , respectively. Inhibition of these compounds was higher than carbofuran and metam sodium but significantly lower than fosthiazate. In contact + fumigant mortality bioassays with J2, EC and EMC applied at 0.25 and 0.125 mg (g soil) −1 resulted in 81 and 80% and 77 and 73% mortality, respectively, while carbofuran and metam sodium treatments resulted in 86 and 96% and 57 and 73% mortality, respectively. Fosthiazate resulted in 92% mortality at 0.063 mg (g soil) −1 . In vapour-phase mortality bioassays with J2, EC and EMC were more effective in a closed container than in an open one, indicating that mode of delivery was, in part, a result of vapour action. Global efforts to reduce the level of highly toxic synthetic nematicides in the agricultural environment justify further studies on K. galanga rhizome-derived materials, particularly ethyl cinnamate and ethyl p-methoxycinnamate, as potential nematicides and hatching inhibitors for the control of M. incognita as fumigants with contact action.
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