Vestibular histofluorescence could be due to accumulation of both the antibiotic and its derivative, streptidine, after acute streptomycin treatment in the guinea pig.

Acute treatment with 300 mg/kg of pigmented guinea pigs with streptomycin sulfate induces an elevation of endogenous fluorescence in vestibular ampullary cristae. Fluorescence accumulates in all compartments of the epithelium, i.e., vestibular sensory and supporting cells and nerve fibers of the stroma and it was very intense 1 and 12 hours after its administration. Fluorescence decreased to control levels 24 hours following streptomycin injection. Fluorescence levels were very low either in untreated animals or in animals injected with saline physiological solution. To investigate whether this fluorescence was an intrinsic property of the antibiotic or whether it was due to a derivative of it, or both, an in vitro fluorescence spectrum was performed with 100 microM solutions of streptomycin or streptidine, or both, dissolved in various buffer solutions at 488 nm of excitation. A discrete level of fluorescence was observed in the spectrum regardless of media when separate solutions of both streptomycin or streptidine were studied. Fluorescence notably increased at 522-532 nm when the solutions contained both streptomycin and streptidine together. These results suggest that streptidine putatively derived from streptomycin may contribute to the observed fluorescence accumulation in vestibular preparations after acute treatment. Thus, these metabolic properties of the inner ear which transform streptomycin into streptidine, something never considered earlier, could be claimed as partially responsible for converting a therapeutic agent into a compound which could be as harmful as STP to the inner ear.

Two inhibition targets by [Cr(2gb)(3)](3+) and [Co(2gb)(3)](3+) on redox enzymes of spinach thylakoids.

[Cr(2gb)(3)]Cl(ZnCl(4)), [Cr(2gb)(3)]Cl(3), and [Co(2gb)(3)]Cl(3) were synthesized and characterized. Their chemical structures and the oxidation states of their metal centers remained unchanged in solution. The effects of these compounds, CrCl(3) and [Co(NH(3))(6)]Cl(3), on photosynthesis were investigated. The coordination compounds inhibit ATP synthesis and electron flow (basal, phosphorylating, and uncoupled), behaving as Hill reaction inhibitors. The target for [Cr(2gb)(3)]Cl(ZnCl(4)) is located at the Q(B) level. In contrast, the interaction sites of [Cr(2gb)(3)]Cl(3) and [Co(2gb)(3)]Cl(3) are located in the span from P(680) to Q(A) and at the b(6)f complex. Neither CrCl(3) nor [Co(NH(3))(6)]Cl(3) inhibited photosynthesis. The 100% inhibition on PS II of [Cr(2gb)(3)]Cl(ZnCl(4)) is explained in terms of a synergystic effect between the 2gb-chromium(III) coordination compound and the ZnCl(4)(2)(-) anion.

Coordination compounds derived from the interaction of streptomycin and cobalt, nickel, copper, and calcium salts characterized by 13C NMR and spectroscopic studies. Structure and bonding properties of the streptidine fraction.

The coordination compounds of streptomycin (St), Co2(St)Cl4.13H2O (2), Co2(St)(NO3)4.7H2O (3), Ni2(St)Cl4.14H2O (4), Ni2(St)(NO3)4.14H2O (5), Cu2(St)Cl4.6H2O (6), and Ca(St)Cl2.8H2O (7) have been synthesized by the reaction of streptomycin sulfate (1) with three equivalents of the corresponding inorganic salt. The compounds (2)-(7) were characterized by electronic spectroscopy (in the solid state and in solution) by conductivity measurements and by 13C NMR in solution. The reaction of streptomycin with CuCl2 in water hydrolyzed the molecule giving the copper complex of the streptidine fraction (Std), Cu(Std)Cl.H2O (8). This compound was characterized by the same techniques. Detailed x-ray diffraction and 13C NMR studies of streptidine sulfate (9) were carried out.