Extensive usage and heavy reliance on insecticides have led to the development of insecticide resistance in the German cockroach, Blattella germanica (L.). Six field-collected strains of B. germanica from Singapore were used to investigate resistance to fipronil and dieldrin. The three strains (Boat Quay, Cavenagh Road, and Ghimmoh Road) with greatest resistance to fipronil were subjected to selection with fipronil bait up to the F5 generation. Synergism assay and molecular detection of a target site mutation were used to elucidate the mechanism of fipronil resistance in these strains. With the exception of the Cavenagh Road strain, all parental strains were susceptible to dieldrin. This strain exhibited resistance to dieldrin and fipronil with resistance ratios of 4.1 and 3.0, respectively. Piperonyl butoxide and S,S,S-tributylphosphorotrithioate were antagonistic toward fipronil toxicity in all strains. Bait selection significantly increased fipronil and dieldrin resistance in the three chosen strains, either in topical bioassay or bait evaluations. There was a significant positive relationship [y = (6,852.69 +/- 1,988.37) x - (708.93 +/- 1,226.28), where x = fipronil toxicity and y = dieldrin toxicity] between dieldrin and fipronil resistance levels, indicating significant cross-resistance between the insecticides. High frequencies of individuals possessing the Rdl gene mutation were found in the F5 generation of the three strains selected with fipronil bait. The synergism assays indicated that monooxygenase and esterase were not involved in fipronil resistance in the strains studied herein. The A302S Rdl mutation was the major mechanism contributing to fipronil and dieldrin resistance in these strains.
This study was carried out in mice to determine the nonopioid receptor signaling pathway(s) that might modulate the antinociceptive activity of the aqueous and chloroform extracts of Muntingia calabura (M. calabura) leaves, using the hot-plate test. The leaves of M. calabura were sequentially soaked [1:2 (w/v); 72 h] in distilled water (dH(2)O) and chloroform. The 50% concentration extracts were selected for this study based on the plant's previously established antinociceptive profiles. The mice (n = 7) were pretreated (s.c.) for 10 min with the selected nonopioid receptor antagonists, followed by the (s.c.) administration of the respective extract. The latency of discomfort was recorded at the interval time of 0.5, 1, 2, 3, 4 and 5 h after the extract administration. The 5 mg/kg atropine, 10 mg/kg phenoxybenzamine, 10 mg/kg yohimbine, 10 mg/kg pindolol, 1 mg/kg haloperidol and 10 mg/kg bicuculline caused significant (p < 0.05) reduction in the aqueous extract-induced antinociceptive activity. The 10 mg/kg phenoxybenzamine, 10 mg/kg yohimbine, 10 mg/kg pindolol and 10 mg/kg bicuculline caused significant (p < 0.05) reduction in the chloroform extract-induced antinociceptive activity. In conclusion, the central antinociceptive activity of M. calabura leaves appears to be involved in the modulation of various nonopioid receptor signaling pathways. Its aqueous extract antinociceptive activity is mediated via modulation of the muscarinic, alpha(1)-adrenergic, alpha(2)-adrenergic, beta-adrenergic, dopaminergic and GABAergic receptors, while its chloroform extract activity is mediated via modulation of the alpha(1)-adrenergic, alpha(2)-adrenergic, beta-adrenergic and GABAergic receptors.