Melatonin protects against copper‐mediated free radical damage
- Parmar, Paresh, Limson, Janice L, Nyokong, Tebello, Daya, Santy
- Authors: Parmar, Paresh , Limson, Janice L , Nyokong, Tebello , Daya, Santy
- Date: 2002
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/289617 , vital:56654 , xlink:href=" https://doi.org/10.1034/j.1600-079X.2002.01859.x"
- Description: Copper is an essential trace element which forms an integral component of many enzymes. While trace amounts of copper are needed to sustain life, excess copper is extremely toxic. Copper has been implicated in various neurodegenerative disorders, such as Wilson's and Alzheimer's diseases. Previous studies showed that melatonin, the principle secretory product of the pineal gland, binds Cupric chloride (Cu2+) and that this may have implications in copper-induced neurodegenerative diseases. In the present study, in vitro copper-mediated lipid peroxidation was induced. Melatonin (5 mM) protected against copper-mediated lipid peroxidation in liver homogenates. Electron micrographs of in vivo administered Cu2+ and melatonin show that melatonin affords some protection to rat hepatocytes in the presence of copper. Electrochemical studies performed show that melatonin, in addition to binding Cu2+, may provide protection against copper-mediated free radical damage by binding Cu1+. The findings of these studies provide further evidence for the neuroprotective role of melatonin.
- Full Text:
- Date Issued: 2002
- Authors: Parmar, Paresh , Limson, Janice L , Nyokong, Tebello , Daya, Santy
- Date: 2002
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/289617 , vital:56654 , xlink:href=" https://doi.org/10.1034/j.1600-079X.2002.01859.x"
- Description: Copper is an essential trace element which forms an integral component of many enzymes. While trace amounts of copper are needed to sustain life, excess copper is extremely toxic. Copper has been implicated in various neurodegenerative disorders, such as Wilson's and Alzheimer's diseases. Previous studies showed that melatonin, the principle secretory product of the pineal gland, binds Cupric chloride (Cu2+) and that this may have implications in copper-induced neurodegenerative diseases. In the present study, in vitro copper-mediated lipid peroxidation was induced. Melatonin (5 mM) protected against copper-mediated lipid peroxidation in liver homogenates. Electron micrographs of in vivo administered Cu2+ and melatonin show that melatonin affords some protection to rat hepatocytes in the presence of copper. Electrochemical studies performed show that melatonin, in addition to binding Cu2+, may provide protection against copper-mediated free radical damage by binding Cu1+. The findings of these studies provide further evidence for the neuroprotective role of melatonin.
- Full Text:
- Date Issued: 2002
The interaction of melatonin and its precursors with aluminium, cadmium, copper, iron, lead, and zinc
- Limson, Janice L, Nyokong, Tebello, Daya, Santy
- Authors: Limson, Janice L , Nyokong, Tebello , Daya, Santy
- Date: 1998
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/293323 , vital:57075 , xlink:href="https://doi.org/10.1111/j.1600-079X.1998.tb00361.x"
- Description: Melatonin, a pineal secretory product, and its precursors, tryptophan and serotonin, were examined for their metal binding affinities for both essential and toxic metals: aluminium, cadmium, copper, iron, lead, and zinc. An electrochemical technique, adsorptive stripping voltammetry, showed the varying abilities of melatonin and its precursors to bind the metals in situ. The results show that the following metal complexes were formed: aluminium with melatonin, tryptophan, and serotonin; cadmium with melatonin and tryptophan; copper with melatonin and serotonin; iron(III) with melatonin and serotonin; lead with melatonin, tryptophan, and serotonin; and zinc with melatonin and tryptophan. Iron(II) showed the formation of an in situ complex with tryptophan only. These studies suggest a further role for melatonin in the reduction of free radical generation and metal detoxification, and they may explain the accumulation of aluminium in Alzheimer's disease.
- Full Text:
- Date Issued: 1998
- Authors: Limson, Janice L , Nyokong, Tebello , Daya, Santy
- Date: 1998
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/293323 , vital:57075 , xlink:href="https://doi.org/10.1111/j.1600-079X.1998.tb00361.x"
- Description: Melatonin, a pineal secretory product, and its precursors, tryptophan and serotonin, were examined for their metal binding affinities for both essential and toxic metals: aluminium, cadmium, copper, iron, lead, and zinc. An electrochemical technique, adsorptive stripping voltammetry, showed the varying abilities of melatonin and its precursors to bind the metals in situ. The results show that the following metal complexes were formed: aluminium with melatonin, tryptophan, and serotonin; cadmium with melatonin and tryptophan; copper with melatonin and serotonin; iron(III) with melatonin and serotonin; lead with melatonin, tryptophan, and serotonin; and zinc with melatonin and tryptophan. Iron(II) showed the formation of an in situ complex with tryptophan only. These studies suggest a further role for melatonin in the reduction of free radical generation and metal detoxification, and they may explain the accumulation of aluminium in Alzheimer's disease.
- Full Text:
- Date Issued: 1998
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