Publications by authors named "S J Bellin"

The reaction between glutathione and 2,5-diaziridinyl-1,4-benzoquinones bearing halogen substituents at C3 and C6 was examined in terms of the formation of glutathionyl-quinone conjugates and semiquinones by HPLC with UV detection, mass spectroscopy and EPR. The reactivity of the halogen atoms toward sulfur substitution is the primary reaction leading to the formation of mono- and di-glutathionyl-substituted quinones. The relative formation of these conjugates depended on the GSH/quinone molar ratios.

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In electrically driven guinea pig left atria, plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone; 0.5-10 microM) produced a marked positive inotropic effect that was about 65% that caused by isoprenaline in the same experimental conditions. The effect was mainly not dependent on catecholamine release from adrenergic stores.

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1. Three benzoquinones (p-benzoquinone, 2,5-dimethyl-p-benzoquinone and tetramethyl-1,4-benzoquinone), differing for their electrophilicity, were tested on Ca2+ ATPase activity of cardiac sarcoplasmic reticulum membrane vesicles. 2.

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Four naphthoquinones (5-OH-1,4-naphthoquinone (juglone), 5-OH-2-CH3-1,4-naphthoquinone (plumbagine), 2-CH3-1,4-naphthoquinone (menadione) and 2,3-(OCH3)2-1,4-naphthoquinone (2,3diOmeNQ)), differing for the presence of electrophilic groups in orto position in respect of quinone mojety and for hydroxylation in C5, were tested on Ca2+ ATPase activity of cardiac sarcoplasmic reticulum membrane vesicles. The 2-unsubstituted quinone, juglone, was a potent inhibitor of Ca2+ ATPase activity, while the 2-methyl-substituted quinones, plumbagine and menadione, inhibited the enzyme activity only after a sufficiently long preincubation time 2,3DiOMeNQ did not affect Ca2+ ATPase activity at all. Hydroxylation in C5 was responsible for the type of inhibition, making it irreversible.

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To test the working hypothesis that neurosecretory neuronal regeneration is largely dependent on microenvironmental conditions at the lesion site, intact or predegenerated optic nerves were allografted intrahypothalamically into the hypothalamo-neurohypophysial tract. Neurosecretory axons regenerated consistently into all grafts. Early regeneration proceeded without glial cell association.

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