The acid-catalysis of chromic acid oxidation of carboxymethyl cellulose (CMC) as a polysaccharide in aqueous perchlorate solutions at a constant ionic strength of 2.0 mol dm−3 have been investigated spectrophotometrically. The experimental results showed first-order kinetics in chromic acid and fractional first-order dependence with respect to [CMC]. A kinetic evidence for the formation of 1:1 complex between chromic acid and CMC was revealed. The hydrogen ion dependence of the reaction rates showed that the oxidation process is acid-catalyzed. Induced polymerization of acrylonitrile indicated that the oxidation process proceeds by free-radical mechanism. The kinetic parameters have been evaluated and a tentative reaction mechanism consistent with the kinetic results is suggested.

The acid-catalysis of chromic acid oxidation of carboxymethyl cellulose (CMC) as a polysaccharide in aqueous perchlorate solutions at a constant ionic strength of 2.0 mol dm−3 have been investigated spectrophotometrically. The experimental results showed first-order kinetics in chromic acid and fractional first-order dependence with respect to [CMC]. A kinetic evidence for the formation of 1:1 complex between chromic acid and CMC was revealed. The hydrogen ion dependence of the reaction rates showed that the oxidation process is acid-catalyzed. Induced polymerization of acrylonitrile indicated that the oxidation process proceeds by free-radical mechanism. The kinetic parameters have been evaluated and a tentative reaction mechanism consistent with the kinetic results is suggested.

The acid-catalysis of chromic acid oxidation of carboxymethyl cellulose (CMC) as a polysaccharide in aqueous perchlorate solutions at a constant ionic strength of 2.0 mol dm−3 have been investigated spectrophotometrically. The experimental results showed first-order kinetics in chromic acid and fractional first-order dependence with respect to [CMC]. A kinetic evidence for the formation of 1:1 complex between chromic acid and CMC was revealed. The hydrogen ion dependence of the reaction rates showed that the oxidation process is acid-catalyzed. Induced polymerization of acrylonitrile indicated that the oxidation process proceeds by free-radical mechanism. The kinetic parameters have been evaluated and a tentative reaction mechanism consistent with the kinetic results is suggested.

The acid-catalysis of chromic acid oxidation of carboxymethyl cellulose (CMC) as a polysaccharide in aqueous perchlorate solutions at a constant ionic strength of 2.0 mol dm−3 have been investigated spectrophotometrically. The experimental results showed first-order kinetics in chromic acid and fractional first-order dependence with respect to [CMC]. A kinetic evidence for the formation of 1:1 complex between chromic acid and CMC was revealed. The hydrogen ion dependence of the reaction rates showed that the oxidation process is acid-catalyzed. Induced polymerization of acrylonitrile indicated that the oxidation process proceeds by free-radical mechanism. The kinetic parameters have been evaluated and a tentative reaction mechanism consistent with the kinetic results is suggested.

The oxidative status and the morphological changes of liver of rats exposed to cadmium (5 mg Cd/kg
body weight subcutaneously) for 22 days and the protective role of melatonin (10 mg/kg b.w.) against
the toxicity of cadmium was studied. The concentration of malondialdehyde (MDA), as an indicator
of lipid peroxidation, activity of the antioxidant enzyme superoxide dismutase (SOD) as well as the
concentration of glutathione (GSH) was measured in the liver. The morphological changes were
investigated using both light and electron microscopes. The exposure to Cd led to an increase of MDA
levels and a decrease of both the activity of SOD and GSH concentration in the liver. In contrast,
melatonin administration restored the previous changes to nearly the normal levels. Morphologically,
Cd led to different histopathological changes such as loss of normal architecture of the parenchymatous
tissue, cytoplasmic vacuolization, cellular degeneration and necrosis, congested blood vessels,
destructed cristae mitochondria, fat globules, severe glycogen depletion, lipofuscin pigments, and
collagenous fibers formation. Again, melatonin administration counteracts all changes and the tissue
appears more or less normal. The rate of recovery was faster when melatonin was administered for
treatment after the exposure to cadmium than if the animals left without any treatment. The results
suggest that melatonin may be useful as an antioxidant in combating free radical-induced oxidative
stress and tissue injury that is a result of cadmium toxicity.

The oxidative status and the morphological changes of liver of rats exposed to cadmium (5 mg Cd/kg
body weight subcutaneously) for 22 days and the protective role of melatonin (10 mg/kg b.w.) against
the toxicity of cadmium was studied. The concentration of malondialdehyde (MDA), as an indicator
of lipid peroxidation, activity of the antioxidant enzyme superoxide dismutase (SOD) as well as the
concentration of glutathione (GSH) was measured in the liver. The morphological changes were
investigated using both light and electron microscopes. The exposure to Cd led to an increase of MDA
levels and a decrease of both the activity of SOD and GSH concentration in the liver. In contrast,
melatonin administration restored the previous changes to nearly the normal levels. Morphologically,
Cd led to different histopathological changes such as loss of normal architecture of the parenchymatous
tissue, cytoplasmic vacuolization, cellular degeneration and necrosis, congested blood vessels,
destructed cristae mitochondria, fat globules, severe glycogen depletion, lipofuscin pigments, and
collagenous fibers formation. Again, melatonin administration counteracts all changes and the tissue
appears more or less normal. The rate of recovery was faster when melatonin was administered for
treatment after the exposure to cadmium than if the animals left without any treatment. The results
suggest that melatonin may be useful as an antioxidant in combating free radical-induced oxidative
stress and tissue injury that is a result of cadmium toxicity.