| Reference | <p style=/line-height:25px/>
<br>[1]. Gao H, Liu M, Liu J, Dai H, Zhou X, Liu X, Zhuo Y, Zhang W, Zhang L. Medium optimization for the production of avermectin B1a by Streptomyces avermitilis 14-12A using response surface methodology. Bioresour Technol. 2009 Sep;100(17):4012-6.
Abstract
Response surface methodology was employed to optimize the composition of medium for the production of avermectin B1a by Streptomyces avermitilis 14-12A in shaker flask cultivation. Corn starch and yeast extract were found to have significant effects on avermectin B1a production by the Plackett-Burman design. The steepest ascent method was used to access the optimal region of the medium composition, followed by an application of response surface. The analysis revealed that the optimum values of the tested variables were 149.57 g/l corn starch and 8.92 g/l yeast extract. A production of 5128 mg/l, which was in agreement with the prediction, was observed in verification experiment. In comparison to the production of original level (3528 mg/l), 1.45-fold increase had been obtained.
<br>[2]. Sun Y, Diao X, Shen J. Effects of avermectin B1a on soil microorganism and earthworm (Eisenia fetida).Ying Yong Sheng Tai Xue Bao. 2005 Nov;16(11):2140-3.
Abstract
Avermectins are the pesticides widely applied in agriculture. This paper studied the effects of different concentration avermectin B1a (AVM B1a) on soil bacteria and fungi, soil respiration, and soil earthworm (Eisenia fetida). The results showed that in 4 test soils, bacteria were significantly inhibited when the AVM B1a concentration was higher than 83.3 mg x kg(-1), while fungi were less impaired. Soil respiration was also inhibited by high concentration AVM B1a, which differed with soil types. The half lethal dosage (LD50) of AVM B1a to soil earthworm was estimated as 4.63 microg x cm(-2) in filter paper contact test, and as 24.13 and 17.06 mg x kg(-1), respectively after treated 7 and 14 days in artificial soil.
<br>[3]. Sun Y, Diao X, Zhang Q, Shen J. Bioaccumulation and elimination of avermectin B1a in the earthworms (Eisenia fetida). Chemosphere. 2005 Jul;60(5):699-704.
Abstract
The acute toxicity, bioaccumulation, and elimination of avermectin B1a (AVM B1a) in earthworm (Eisenia fetida) were investigated in different exposure systems. The LC50 of AVM B1a on earthworms were 24.1 mg/kg and 17.1 mg/kg, respectively, for 7 and 14 days in artificial soil. The LC50 tested by the filter paper for 2 days was 4.63 microg/cm2. The earthworms were cultivated in artificial soil containing 0.6 mg/kg and 3.0 mg/kg AVM B1a, respectively for bioaccumulation experiments. The AVM B1a residues in earthworms were determined with HPLC-fluorescence method. The results showed that AVM B1a was taken up from the concentrated artificial soil by the earthworms and the steady-state levels were reached after 9-18 days of exposure. On the 18th day, the final concentrations of AVM B1a in the earthworms treated with two different dosages were 107 ng/g and 165 ng/g, respectively; there were not significantly accumulation. About 80.0% and 94.8% of the accumulated AVM B1a were eliminated respectively in two groups within 1 day after they were exposed to AVM B1a-free soil, but a trace amount of AVM B1a was found for a relative long time in earthworms.
<br>[4]. Huang J, Casida JE. Avermectin B1a binds to high- and low-affinity sites with dual effects on the gamma-aminobutyric acid-gated chloride channel of cultured cerebellar granule neurons. J Pharmacol Exp Ther. 1997 Apr;281(1):261-6.
Abstract
Avermectin B1a (AVM B1a), a widely used insecticide and acaricide, is reported to both activate and inhibit gamma-aminobutyric acidA (GABA(A)) receptor function in mammalian brain. This study attempts to resolve these seemingly contradictory results by examining the binding properties of AVM B1a and its effects on the GABA-gated chloride channel with primary cultures of rat cerebellar granule neurons as a model system. Specific binding of [3H]AVM B1a in intact neuron cultures is time- and concentration-dependent and is displaceable by AVM analogs. Scatchard analysis of [3H]AVM B1a binding reveals high- and low-affinity sites with K(D) values of 5 and 815 nM, respectively. AVM B1a alters the binding of [3H]ethynylbicycloorthobenzoate at the noncompetitive blocker site in a biphasic manner; activation is evident with 10 to 300 nM AVM B1a after 5 to 10 min incubation and inhibition with an IC50 of 866 nM after 60 min incubation. Consistent with this observation, 36Cl- influx is stimulated by AVM B1a at 3 to 100 nM and inhibited at 1 to 3 microM. GABA-stimulated 36Cl- influx is completely blocked by both [3H]ethynylbicycloorthobenzoate and 12-ketoendrin (two GABA-gated chloride channel blockers) and AVM B1a at 1 to 1.5 microM. Also, 36Cl- influx induced by AVM B1a at 10 nM is suppressed by the two channel blockers. Thus, AVM B1a binds to two different sites in the GABA-gated chloride channel with dual effects, i.e., activating the channel on binding to the high-affinity site and blocking it on further binding to the low-affinity site.
<br>[5]. Payne GT, Soderlund DM. Activation of gamma-aminobutyric acid insensitive chloride channels in mouse brain synaptic vesicles by avermectin B1a. J Biochem Toxicol. 1991 Winter;6(4):283-92.
Abstract
The interaction of avermectin B1a (AVMB1a) with mouse brain chloride channels was characterized using a radiochloride efflux assay. The loss of intravesicular chloride from synaptoneurosomes preloaded with 36Cl involved an initial rapid phase followed by a slower phase that approached equilibrium within 10 min. AVMB1a stimulated a 30% loss of intravesicular chloride within the first 2 s of exposure; however, AVMB1a had no effect on the rate of the slower phase of chloride loss. Experiments with lysed synaptoneurosomes showed that both chloride loading and basal and AVMB1a-stimulated chloride release required the presence of intact vesicles. The efflux of 36Cl from mouse brain synaptosomes and the stimulation of efflux by AVMB1a were qualitatively similar to the results obtained with synaptoneurosomes but involved much lower overall levels of chloride loading and release. AVMB1a produced half-maximal stimulation of chloride efflux from synaptoneurosomes at a concentration of 2.1 +/- 0.3 microM and a 35.4 +/- 1.4% maximal loss of intravesicular chloride at saturating concentrations. gamma-Aminobutyric acid (GABA), bicuculline, or the chloride channel blockers picrotoxinin, t-butylbicyclophosphorothionate (TBPS) 4,4/’-diisothiocyanatostilbene-2,2/’-disulfonic acid (DIDS), and anthracene 9-carboxylic acid (9-CA) had little or no effect on the loss of chloride from synaptoneurosomes either in the presence or the absence of AVMB1a. However, the chlorinated cycloalkane insecticides dieldrin and lindane were equally effective as inhibitors of GABA-dependent chloride uptake and AVMB1a-stimulated chloride efflux. These data demonstrate that AVMB1a-stimulated chloride efflux from mouse brain synaptic vesicles results from the activation of GABA-insensitive chloride channels and that this action is distinct from their previously documented effects on GABA-gated chloride channels in mouse brain preparations. Our findings imply that both GABA-gated and GABA-insensitive chloride channels may be toxicologically significant targets for the action of avermectins.
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