Behaviors of biomass and kinetic parameter for nitrifying species in A²O process at different sludge retention time.

The effect of sludge retention time (SRT) on biomass, kinetic parameters, and stoichiometric parameters of ammonia-oxidizing bacteria (AOB) and nitrite-oxidizing bacteria (NOB) in anaerobic/anoxic/oxic (A(2)O) process were explored in this study. The results showed that the growth rate constants were 1.52, 1.22, and 0.85 day(-1), respectively, for AOB, those were 1.59, 1.19, and 0.87 day(-1), respectively, for NOB when SRT was 20, 10, and 5 days. The lysis rate constants of AOB and NOB were 0.14 and 0.09 day(-1), respectively. The yield coefficients were 0.23 and 0.22, respectively, for AOB and NOB. They did not change with SRT obviously. The biomass of AOB was 50.94, 26.35, and 14.68 mg L(-1), respectively, and the biomass of NOB was 116.77, 60.00, and 44.25 mg L(-1), respectively, at SRT of 20, 10, and 5 days. When SRT diminished from 20 to 5 days, the biomass of AOB and NOB diminished by 36.26 and 75.52 mg L(-1), respectively. The removal efficiency of NH4 (+)-N diminished by 68.9 %. The removal efficiency of total nitrogen diminished by 42.9 %.

Two new species of Digamasellidae from Taiwan (Acari: Mesostigmata).

This paper reports the occurrence of two new species of Digamasellidae from Taiwan, Dendroseius vulgaris n. sp. and Dendrolaelaps (Foveodendrolaelaps) linjianzheni n. sp. Dendroseius vulgaris is described based on the morphology of adult females, adult males and deutonymph, and D. linjianzheni is based on the morphology of adult females and males. This is the first report on the mite species of Digamasellidae from Taiwan. 

Cardiovascular effects of herbicides and formulated adjuvants on isolated rat aorta and heart.

Various formulations of agricultural chemicals, including solutions, wettable powders, and emulsifiable concentrates, contain adjuvants of solvents and surfactants in addition to active ingredients. Among these formulations, herbicides are among the most commonly used pesticides globally. Some pesticides have been demonstrated to cause severe circulatory failure in poisoned humans. To clarify the potential risk of herbicides and their adjuvants influence on the cardiovascular system, four technical grade (TG) herbicides and their end products (EP), including paraquat, glyphosate, glufosinate, and atrazine, as well as their formulated adjuvants isopropylamine (IPA), polyoxyethylene alkylether sulfate (AES), ethyl acetate (EA), xylene, petrolium-170 (P-170), and solvesso-100 (S-100), were assessed to determine their effects on isolated rat aorta and heart. The results revealed that the vasorelaxation effects of the herbicide EPs exceeded those of TGs, and atrazine produced more significant vasorelaxation in rat aortas than the other herbicides tested. The formulated adjuvants of IPA did not affect the aorta; however, AES, EA, xylene, P-170 and S-100 caused significant vasorelaxation. Herbicide EPs-induced vasorelaxation was generally endothelium-dependent. Furthermore, the TG and EP of paraquat, and the TG of glufosinate and glyphosate were found to have no effect on the isolated heart. However, the normal twitch tensions of the isolated heart were significantly inhibited by EPs of glyphosate and glufosinate, and by TG and EP of atrazine. Although, the adjuvants of IPA appeared unaffected, however, AES, EA, xylene, P-170 and S-100 caused complete inhibition and contraction on the isolated hearts. These results indicated that the adjuvants of herbicides might enhance hypotension and contributed to cardiovascular disorders during intoxication.

Cartap-induced cytotoxicity in mouse C2C12 myoblast cell line and the roles of calcium ion and oxidative stress on the toxic effects.

Our previous study has demonstrated that instead of neuromuscular blockage cartap, an organonitrogen insecticide, could cause a marked irreversible Ca2+-dependent contracture in both isolated mouse and rabbit phrenic nerve-diaphragms. We further examined the potential of direct myocytotoxicity of cartap and the possible roles of calcium ion and oxidative stress on cartap-induced muscle cell injury using the mouse myoblast cell line, C2C12. Cartap exerted a dose- and time-dependent cytotoxic effect in C2C12 cells measured by MTT colorimetric assay and trypan blue dye exclusion. The extracellular activities of both creatine kinase (CK) and lactate dehydrogenase (LDH) were elevated in the cartap-treated groups at or greater than 100 microM. The isoenzymatic profiles showed that the elevations were mainly due to CK-3, LDH-3, and LDH-4. Following the addition of 0.5-2.5mM EGTA, a Ca2+ chelator, or 30-100 microM verapamil, an L-type Ca2+ channel blocker, the cartap-induced reduction in MTT metabolic rate of C2C12 cells was significantly restored in a dose-dependent manner in both EGTA and verapamil-treated cells. Furthermore, EGTA could significantly reduce the cartap-induced elevation in the levels of total extracellular CK and LDH activities. Additionally, cartap significantly increased the level of endogenous reactive oxygen species (ROS) in C2C12 cells in a dose- and time-dependent manner. The cartap-induced ROS generation could be significantly inhibited by antioxidants, including Vitamins C and E, catalase, and superoxide dismutase, with catalase the most effective. EGTA could significantly inhibit cartap-induced ROS generation in a dose-dependent manner. The results suggested that cartap could induce ROS generation in C2C12 cells via a Ca2+-dependent mechanism resulting in subsequent cytotoxicity, at least partially, to C2C12 cells. It is speculated that both Ca2+ and Ca2+-induced ROS may also play the central role on the myogenic contracture and myofiber injury of the diaphragm leading to respiratory failure and subsequent death in rabbits exposed ocularly to cartap.

Endocrine-disrupting activity in carbendazim-induced reproductive and developmental toxicity in rats.

This study was designed to investigate the endocrine-disrupting activity of carbendazim-induced reproductive and developmental toxicity in Sprague-Dawley rats treated orally with the fungicide. Cotreatment of male rats with 675 mg/kg carbendazim and 50 or 100 mg/kg flutamide, an androgen receptor antagonist, once daily for 28 d blocked decrease of testis weight induced by treatment with carbendazim alone. The cotreatment prevented losses of spermatozoa and cell morphology and decrease of sperm concentration induced by carbendazim. Premating treatment of male and female rats with 200 mg/kg carbendazim for 28 d produced androgenic effects including incomplete development of uterine horn, enlargement of uretha, absence of vagina, and induction of seminal vesicles in female offspring, without marked effects in male offspring. Premating treatment with 100mg/kg benomyl, the parent compound of carbendazim, resulted in incomplete development of uterine horn and absence of vagina in female offspring and produced testis and epidydimis atropy in male offspring. Treatment of male rats with 25, 50, 100, 200, 400, and 800 mg/kg carbendazim for 56 d produced dose-dependent increases of androgen receptor concentrations in testis and epididymis. Additions of 5, 50, and 500 microM carbendazim to testis extract from untreated rats replaced binding of [3H]-5 alpha-dihydrotestosterone to androgen receptor in a concentration-dependent manner. The present study demonstrates that reproductive toxicity induced by carbendazim is blocked by an androgen receptor antagonist in male rats and developmental toxicity of the fungicide shows androgenic properties in female offspring. These results suggest that androgen- and androgen receptor-dependent mechanisms are possibly involved in carbendazim-induced toxicity.

Effects of surfactant micelles on viscosity and conductivity of poly(ethylene glycol) solutions.

The neutral polymer-micelle interaction is investigated for various surfactants by viscometry and electrical conductometry. In order to exclude the well-known necklace scenario, we consider aqueous solutions of low molecular weight poly(ethylene glycol) (2-20)x10(3), whose radial size is comparable to or smaller than micelles. The single-tail surfactants consist of anionic, cationic, and nonionic head groups. It is found that the viscosity of the polymer solution may be increased several times by micelles if weak attraction between a polymer segment and a surfactant exists, epsilon

Effect of thuringiensin on adenylate cyclase in rat cerebral cortex.

The purpose of this work is to evaluate the effect of thuringiensin on the adenylate cyclase activity in rat cerebral cortex. The cyclic adenosine 3'5'-monophosphate (cAMP) levels were shown to be dose-dependently elevated 17-450% or 54-377% by thuringiensin at concentrations of 10 microM-100 mM or 0.5-4 mM, due to the activation of basal adenylate cyclase activity of rat cerebral cortical membrane preparation. Thuringiensin also activated basal activity of a commercial adenylate cyclase from Escherichia coli. However, the forskolin-stimulated adenylate cyclase activity in rat cerebral cortex was inhibited by thuringiensin at concentrations of 1-100 microM, thus cAMP production decreased. Furthermore, thuringiensin or adenylate cyclase inhibitor (MDL-12330A) reduced the forskolin (10 microM)-stimulated adenylate cyclase activity at concentrations of 10 microM, 49% or 43% inhibition, respectively. In conclusion, this study demonstrated that thuringiensin could activate basal adenylate cyclase activity and increase cAMP concentrations in rat cerebral cortex or in a commercial adenylate cyclase. Comparing the dose-dependent effects of thuringiensin on the basal and forskolin-stimulated adenylate cyclase activity, thuringiensin can be regarded as a weak activator of adenylate cyclase or an inhibitor of forskolin-stimulated adenylate cyclase.

Susceptibility to cartap-induced lethal effect and diaphragmatic injury via ocular exposure in rabbits.

Cartap is extensively used to control agricultural pests. Pertinent literatures have indicated that it causes no eye irritation [D.E. Ray, Insecticides derived from plants and other organisms, in: W.J. Hayes, E.R. Laws (Eds.), Handbook of Insecticide Toxicology, Classes of Insecticides, vol. 2, Academic Press, New York, 1991, p. 611; C. Tomlin, Cartap, in: C. Tomlin (Ed.), The Insecticide Manual, 12th ed., British Crop Protection Council, Surrey, UK, 2000, p. 144]; however, the instillation of a little cartap through the eye has caused death in rabbits. The aim of this study was to determine the ocular toxicity of cartap in New Zealand White rabbits. Cartap was directly instilled into the low conjunctival sac of eyes, at doses of 0, 5, 7.5, 10 and 12.5 mg/kg body weight. The changes in the enzymes and isoenzymes of creatine kinase (CK), lactate dehydrogenase (LD), as well as pathological changes in the muscles of the heart, thigh and diaphragm were determined in the cartap-treated rabbits. Moreover, the neuromuscular effect of cartap was examined using the isolated rabbit phrenic-nerve diaphragm model. The results indicated that rabbits developed severe signs and they died within 20 min of ocular instillation. The ocular LD50 of cartap was 8.1 mg/kg body weight. Treatment with cartap increased the activities of CK and LD enzymes and their isoenzymes, CK-1, CK-2, and CK-3 in serum, and CK-3 and LD-5 in the diaphragm. Microscopically, hypercontraction bands and the rupture of myofibers of the diaphragm were observed in dead rabbits. Cartap did not affect nerve-evoked twitch but induced irreversible contracture and twitch depression on the isolated rabbit's diaphragm. These results indicate that the rabbit is susceptible to cartap toxicity; the effect of cartap caused contracture and damage to the diaphragm might play a pivotal role in respiratory paralysis and death of rabbits during intoxication.

Pulmonary toxicity of thuringiensin administered intratracheally in Sprague-Dawley rats.

The purpose of this work is to evaluate the pulmonary toxicity of purified thuringiensin in Sprague-Dawley rats. Rats were intratracheally instillated with 0, 0.4, 0.8, 1.6, 3.2, 6.4 and 9.6 mg/kg body weight of thuringiensin. The results indicated that the acute pulmonary LD(50) of thuringiensin for rats was 4.4 mg/kg. The total number of inflammatory cells and lactate dehydrogenase (LDH) activity in the bronchoalveolar lavage (BAL) fluid increased in a dose-dependent manner after thuringiensin instillation. Furthermore, an effective dose of 1.6 mg/kg was selected for the time course study of pulmonary toxicity. The treated animals showed a significant increase in the weights of the lungs, hydroxyproline levels in the lungs and total number of cells in BAL fluid 2, 4, 7, 14, 28 and 56 days after treatment. In comparison with the control, the total protein concentrations in BAL fluid were increased by 361, 615, 116, 41, 34 and 41%, after 2, 4, 7, 14, 28 and 56 days, respectively. The LDH activity in BAL fluid showed a significant increase after 1, 2, 4, 7, 14, 28 and 56 days. The increases in fibronectin levels were 164, 552, 490, 769, 335, 257 and 61% at the corresponding times, but neither tumor necrosis factor nor interleukin-1 increased. The treated rats presented abnormal histology including distributed inflammation in the bronchioles and alveoli, bronchial cellular necrosis on days 1 and 2, and areas of septal thickening with cellular infiltration and collagen deposit in the intestinal and alveolar spaces on days 4-56. Based on these biochemical and pathological parameters, intratracheal instillation of purified thuringiensin might cause significant pulmonary toxicity in rats.