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Angiotensin II (AII), injected intracerebroventricularly, has been shown to antagonize opioid analgesia. The mechanism for this was obscure. In the neuroblastoma X glioma NG 108-15 hybrid cell line, the K(+)-induced increase in [Ca2+]i can be suppressed by the delta opioid agonist [D-Pen2, D-Pen5]enkephalin (DPDPE) at 0.01-1 microM, an effect completely reversed by the opioid antagonist naloxone. Angiotensin II (AII) at concentrations of 0.1 and 1 microM mobilized free Ca2+ from an intracellular pool, and this effect was antagonized by the AII receptor antagonist saralasin. All (1 microM) had no significant effect on the increase in [Ca2+]i induced by K+, but it blocked the suppressive effect of DPDPE on the K(+)-induced [Ca2+]i increase. The results indicate that mobilization of intracellular calcium may underlie the anti-opioid effect of AII.

The efficacy of broad-spectrum anthelmintics in current use was studied in Hengshan County, Hunan Province. The vermicides under study include albendazole (400mg, single dose), mebendazole composite (mebendazole 100 mg and levamisole 25mg bid x 3d), oxantel pyrantel pamoate composite (pyrantel pamoate 150 mg and oxantel pamoate 150 mg bid x 2d), and pyrantel pamoate composite (base 10 mg/kg, single dose). Therapeutic effect assessed 2 weeks after medication revealed Ascaris egg negative rates or cure rates (CR) of 97.5-100% for the former 3 regimens, and 80.9% for the latter one; while CR for hookworm infection were 95.4%, 78.6-100%, 96.7% and 83.3%, respectively. A follow-up survey pursued 4 weeks post treatment showed no significant difference in CR for the above regimens. Judging from CR in Trichuris trichiura infection, pyrantel pamoate composite was recommended as the drug of choice (89.3%), which was followed by mebendazole composite (64.6-83.8%) and albendazole (28.2-42.6%), whereas pyrantel pamoate was inefficacious. Obvious egg reduction rates were evidenced post application of the above drugs in trichuriasis treatment except pyrantel pamoate at single dose.

The following experiments were conducted to evaluate the genotoxic effects of GMA (glycidyl methacrylate) on mammalian and human cells. (1) Using the absorption spectrum shift method in vitro, we observed that the maximums of calf thymus DNA and GMA were shifted toward longer wavelengths (a change of more than 15 nm) and the absorbance decreased after incubation at room temperature for 15 min or more. The result indicates that binding of DNA and GMA had occurred. The binding force is strong, not affected by the addition of concentrated sodium chloride solution, and only slightly decreased by the addition of 8 M urea solution. Therefore the bond between DNA and GMA might be covalent. (2) In cell cultures, unscheduled DNA synthesis (UDS) in human and/or rat lymphocyte was induced and DNA semiconservative replication was inhibited by GMA at concentrations of less than 5.2 mM. (3) Sperm abnormality tests and assays of UDS in germ cells of male mice were conducted to study the in vivo genotoxicity of GMA. The results revealed that GMA could damage DNA, increase sperm abnormality frequency, and reduce the number of sperm cells.

Glycidyl methacrylate (GMA) is a recently recognized chemical mutagen. In order to explore the mutagenicity and mutagenic process of GMA, plasmid pBR322 was used for in vitro binding, mutant screening, and restriction enzyme mapping. The binding between GMA and DNA in vitro has been verified by means of a spectrophotometric method. When pBR322 and GMA-bound pBR322 were used to transform Escherichia coli HB101, the following results were obtained: (1) The transformation efficiency of GMA-bound pBR322 was much lower than that of pBR322 alone. (2) GMA-bound pBR322 induced phenotype changes in competent cells (i.e., tetracycline-resistance inactivation or ampicillin-resistance inactivation). There were two mutants of pBR322, ApRTCS and ApSTcR, in the transformants and a deductive mutant ApsTcs in the nontransformants. (3) All of the selected mutants were stable and heritable. (4) When restriction enzyme maps were used to analyze the mutant ApRTcS, four of seven maps were changed, some sites were shifted to other resistant gene regions, for example, sites of Bg/I, EcoRI, HindIII, HincII, etc., and there was a new recognition site for HincII (252). We did not observe any DNA fragment insertion or deletion on any maps. Our results suggest that when GMA is covalently linked to the plasmid DNA, it gives rise to a premutagenic lesion of DNA that is converted in vivo into a point mutation.

Pseudomonas S-42 was capable of decolorizing azo dyes such as Diamira Brilliant Orange RR(DBO-RR), Direct Brown M (DBM), Eriochrome Brown R(EBR) and so on. The cell suspension, cell-free extract and purified enzyme of Pseud. S-42 could decolorize azo dyes under similar conditions: the optimum pH and temperature laid 7.0 and 37 degrees C respectively. The efficiencies of decolorizing of DBO-RR, DBM, EBR by intact cells stood more than 90%. When the cell concentration was 15 mg(wet)/ml and the reaction time was 5 hours, the decolorizing activity for above three azo dyes by intact cells were 1.75, 2.4, 0.95 micrograms dye/mg cell, respectively. Cell-free extract and purified enzyme could well express the decolorizing activity only under the anaerobic condition and added NADH. Purified enzyme belongs to azoreductase, its molecular weight is about 34,000-2000 daltons, and its Vmax and Km for DBO-RR are 13 mumol.mg protein-1.min-1 and 54 mumol/L. The results of the detection of the biodegrading products of DBO-RR by spectrophotometric and NaNO2 reactional methods showed that the biodegradation of azo dyes was initiated by the reduction cleavage of azo bonds. It was hypothesized that biodegrading metabolism pathway of DBO-RR by Pseudomonas S-42.

The results of the present study have shown no change in the activity of ATPase of the renal cortex of rats administered gossypol for half a year. The Na+, K+-ATPase activity of the cellular membrane of renal cortex of guinea pigs fed with gossypol for 5 or 9 weeks is significantly altered. It seems possible to diminish or to delay the inhibition by allowing the guinea pigs a potassium-rich diet ad libitum. In vitro, gossypol inhibits significantly the activity of ATPase of the brain and the kidney of rats and guinea pigs uncompetitively. However, the inhibition of the ATPase of human fetus kidney is of a mixed type.

It was detected that both NAD(P)H-linked reductase (TNT-Red) and NAD(P)+-linked TNT dehydrogenase (TNT-Deh) were present in TNT-degrading enzymes of Citrobacter freundii simultaneously. The time course of formation for the enzymes and the actions of coenzymes in enzymatic reaction of TNT have been studied. The effects of varied carbon and nitrogen sources on the regulation of the enzymes were different clearly. When the concentration of NH4Cl or urea in culture medium was more than 0.1 mol/L, the formation of both TNT reductase and TNT dehydrogenase was promoted. However, the formation of these enzymes was inhibited by KNO3 in culture. The production of both reductase and dehydrogenase was promoted by glucose. The sodium citrate was able to help the formation of the TNT dehydrogenase. The activity of the TNT reductase was increased when the concentration of sodium citrate was less than 0.5%, but when it was more than 0.5%, the activity of this enzyme was decreased rapidly.