The comprehensive effects of aluminum oxide nanoparticles on the physiology of freshwater microalga Scenedesmus obliquus and it's phycoremediation performance for the removal of sulfacetamide.

Nanoparticles are inevitable byproducts of modern industry. However, the environmental impacts arising from industrial applications of nanoparticles are largely under-reported. This study evaluated the ecotoxicological effects of aluminum oxide nanoparticles (Al2O3NP) and its influence on sulfacetamide (SA) biodegradation by a freshwater microalga, Scenedesmus obliquus. Although Al2O3NP showed limited toxicity effect on S. obliquus, we observed the toxicity attenuation aspect of Al2O3NP in a mixture of sulfacetamide on microalgae. The addition of 100 mg L-1 of Al2O3NP and 1 mg L-1 of SA reduced total chlorophyll by 23.3% and carotenoids by 21.6% in microalgal compared to control. The gene expression study demonstrated that ATPF0C, Lhcb1, HydA, and psbA genes responsible for ATP synthesis and the photosynthetic system were significantly downregulated, while the Tas gene, which plays a major role in biodegradation of organic xenobiotic chemicals, was significantly upregulated at 1 and 100 mg L-1 of Al2O3NP. The S. obliquus removed 16.8% of SA at 15 mg L-1 in 14 days. However, the removal was slightly enhanced (18.8%) at same concentration of SA in the presence of 50 mg L-1 Al2O3NP. This result proves the stability of sulfacetamide biodegradation capacity of S. obliquus in the presence of Al2O3NP co-contamination. The metabolic analysis showed that SA was degraded into simpler byproducts such as sulfacarbamide, sulfaguanidine, sulfanilamide, 4-(methyl sulfonyl)aniline, and N-hydroxy-benzenamine which have lower ecotoxicity than SA, demonstrating that the ecotoxicity of sulfacetamide has significantly decreased after the microalgal degradation, suggesting the environmental feasibility of microalgae-mediated wastewater technology. This study provides a deeper understanding of the impact of nanoparticles such as Al2O3NP on aquatic ecosystems.

Gastrointestinal absorption of sulfaguanidine in neonatal and adult rats.

The pharmacokinetics of sulfaguanidine in rats was studied after its intravenous or oral administration. In adult rats, its elimination from plasma, after intravenous administration of 2.5 or 25 mg/kg doses, could be described by a two-compartment open model, while its plasma concentration after oral administration of 25 mg/kg doses, agreed with the one- or two-compartment open model. Neonatal rats displayed a lower elimination of sulfaguanidine than adult rats. Comparison of the drug's gastrointestinal absorption showed that the maximum plasma concentration after oral administration was significantly higher for neonatal than for adult rats. However, there was no significant difference between the times required to reach maximum plasma concentrations. The area under the plasma concentration-time curve at 0-infinity h was significantly higher for neonatal than for adult rats. The absolute bioavailability (57.86%) in neonatal rats was approximately five times that (12.76%) in adult rats. Thus, sulfaguanidine was poorly absorbed by adult rats, but was efficiently absorbed by immature gastrointestines of neonatal rats.

Effect of synthetic surfactants on drug absorption in the presence of a physiologic surfactant, sodium taurocholate, in rats.

The effect of synthetic surfactants and their binary mixture with a physiologic one, sodium taurocholate (STC), on the intestinal absorption of drugs was examined in rats by using the in situ recirculation technique. Synthetic surfactants investigated in this study were nonionic polysorbate 80 (PS-80), cationic cetyltrimethylammonium bromide (CTAB), and anionic sodium lauryl sulfate (SLS). The surfactant action on the mucosal membrane seemed to be the same magnitude as the stronger one of the two components, except in the case of CTAB, as estimated by the enhancement effect on sulfaguanidine absorption. The action of CTAB was increased in the presence of STC. The action of surfactants in the aqueous solution, an intraluminal action, was examined by using quinine as a model drug. The micellar interaction of the drug with an ionic surfactant, CTAB or SLS, was reduced by the addition of STC, whereas, that with a nonionic surfactant, PS-80, was increased as estimated by a dynamic dialysis technique. The inhibitory effect on quinine absorption was approximately proportional to the degree of the micellar complex formation. Two other model drugs, imipramine and sulfadimethoxine, were further examined and the possible mechanisms of these effects were discussed.

Differences in effects on drug absorption between dihydroxy and trihydroxy bile salts.

The effect of a dihydroxy bile salt, sodium taurodeoxycholate (STDC), on drug absorption from rat small intestine was investigated in comparison with that of trihydroxy one, sodium cholate (STC). The enhancement or inhibitory effects on the absorption of various model drugs by STDC bore similar tendency to those by STC, and the magnitude was greater than the latter. The absorption of sulfaguanidine was enhanced by STDC, which solubilized the phospholipids from the mucosal barrier membrane in addition to the STC-like, or ethylenediaminetetraacetate-like action. STDC inhibited the absorption of sulfadimethoxine contrary to the insignificant effect by STC. The direct action of STDC on the mucosal membrane reduced the absorption in addition to the physicochemical action, such as micellar complex formation. Quinine absorption was inhibited in the presence of STDC, which can be explained by the micellar complex formation. Possible mechanisms of the differences in the effect of STDC and STC were discussed in relation to their micellar properties.

Permeability of selected drugs and chemicals across the blood-testis barrier of the rat.

Physiological studies by Setchell and others have described the existence of a blood-testis barrier (BTB) surrounding the seminiferous tubules of the mammalian testis. These studies were initiated to better define the role of the BTB with regard to the penetration of exogenous chemicals to male germ cells. The rete testis was cannulated in rats and fluid was collected. Test chemicals or drugs were usually administered by continuous i.v. infusion. Permeability of nonelectrolytes of various molecular sizes, acidic compounds with varying partition coefficients and pKalpha values, such as salicylic acid, barbiturates, and sulfonamides, across the BTB were studied. Permeability of nonelectrolytes was demonstrated to be dependent upon their molecular size, suggesting bulk flow through water-filled pores. On the other hand, permeability of acidic drugs with varying pKalpha values depended upon their partition coefficients. Transport of these chemicals from blood to seminferous tubules closely resembled their transport from blood to cerebrospinal fluid. It appears that the BTB is a complex multicellular system composed of membranes surrounding the semiferous tubules and the several layers of spermatogenic cells organized within the tubules, which restrict the permeability to the male germ cells of many foreign compounds. This must be borne in mind when extra-polating data from in vitro mutagenic test systems to man.

The metabolism of four sulphonamides in cows.

1. The metabolism of sulphanilamide, sulphadimidine (4,6-dimethyl-2-sulphanilamidopyrimidine), sulphamethoxazole (5-methyl-3-sulphanilamidoisoxazole) and sulphadoxine (5,6-dimethoxy-4-sulphanilamidopyrimidine) given by intravenous injection has been examined in cows. 2. The sulphonamides were present mainly as unchanged drugs in blood samples collected 2h after administration. 3. The sulphonamides were excreted in the milk partly as unchanged drugs and partly as conjugated metabolites whereas only small amounts were excreted as the N(4)-acetyl derivatives. 4. The unchanged drug and the N(4)-acetyl derivative were the major constituents in urine samples after administration of sulphanilamide, sulphamethoxazole and sulphadoxine. 5. Besides the unchanged drug, the N(4)-acetyl derivative and the conjugated metabolites, three further metabolites of sulphadimidine were isolated from urine samples and identified. They were 5-hydroxy-4,6-dimethyl-2-sulphanilamidopyrimidine, 4-hydroxymethyl-6-methyl-2-sulphanilamidopyrimidine and sulphaguanidine.