Melatonin generates singlet oxygen on laser irradiation but acts as a quencher when irradiated by lamp photolysis
- Maharaj, Deepa S, Molell, H, Antunes, Edith M, Maharaj, Hiren, Maree, D M, Nyokong, Tebello, Glass, Beverley D, Daya, Santy
- Authors: Maharaj, Deepa S , Molell, H , Antunes, Edith M , Maharaj, Hiren , Maree, D M , Nyokong, Tebello , Glass, Beverley D , Daya, Santy
- Date: 2005
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/300335 , vital:57917 , xlink:href="https://doi.org/10.1111/j.1600-079X.2004.00185.x"
- Description: Melatonin, a naturally occurring chemical mediator, although assigned a diverse range of functions, has attracted interest in recent years because of its ability to function as a free radical scavenger. Because of the implications of singlet oxygen in neurotoxicity, the objective of the study was to investigate the ability of melatonin to quench singlet oxygen generated using laser irradiation or lamp photolysis. The results show that melatonin produces radicals upon laser irradation while the lamp photolysis studies show that melatonin is able to scavenge singlet oxygen produced by naphthalene. While melatonin is a free radical scavenger under biological conditions, it acts as a generator of singlet oxygen and or radicals (as ΦΔ is 1.41) when irradiated with laser light, implying that it has the potential to be used in photodynamic therapy in the destruction of tumors.
- Full Text:
- Date Issued: 2005
- Authors: Maharaj, Deepa S , Molell, H , Antunes, Edith M , Maharaj, Hiren , Maree, D M , Nyokong, Tebello , Glass, Beverley D , Daya, Santy
- Date: 2005
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/300335 , vital:57917 , xlink:href="https://doi.org/10.1111/j.1600-079X.2004.00185.x"
- Description: Melatonin, a naturally occurring chemical mediator, although assigned a diverse range of functions, has attracted interest in recent years because of its ability to function as a free radical scavenger. Because of the implications of singlet oxygen in neurotoxicity, the objective of the study was to investigate the ability of melatonin to quench singlet oxygen generated using laser irradiation or lamp photolysis. The results show that melatonin produces radicals upon laser irradation while the lamp photolysis studies show that melatonin is able to scavenge singlet oxygen produced by naphthalene. While melatonin is a free radical scavenger under biological conditions, it acts as a generator of singlet oxygen and or radicals (as ΦΔ is 1.41) when irradiated with laser light, implying that it has the potential to be used in photodynamic therapy in the destruction of tumors.
- Full Text:
- Date Issued: 2005
Indomethacin reduces lipid peroxidation in rat brain homogenate by binding Fe2+
- Anoopkumar-Dukie, Shailendra, Lack, Barbara, McPhail, Kerry L, Nyokong, Tebello, Lambat, Zaynab, Maharaj, Deepat, Daya, Santy
- Authors: Anoopkumar-Dukie, Shailendra , Lack, Barbara , McPhail, Kerry L , Nyokong, Tebello , Lambat, Zaynab , Maharaj, Deepat , Daya, Santy
- Date: 2003
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/304763 , vital:58487 , xlink:href="https://doi.org/10.1023/A:1021958016928"
- Description: One of the hallmarks of Alzheimer's disease (AD) is the progressive degeneration of cholinergic neurons in the cerebral cortex and hippocampus. It is generally accepted that this neuronal degeneration is due to free-radical-induced damage. These free radicals attack vital structural components of the neurons. This implies that agents that reduce free radical generation could potentially delay the progression of AD. Free radical generation in the brain is assisted by the presence of iron, required by the Fenton reaction. Thus, agents that reduce iron availability for this reaction could potentially reduce free radical formation. Since non steroidal anti-inflammatory drugs (NSAIDS) have been shown to reduce the severity of AD, we investigated the possible mechanism by which indomethacin could afford neuroprotection. Our results show that indomethacin (1 mM) is able to reduce the iron-induced rise in lipid peroxidation in rat brain homogenates. In addition, our NMR data indicate that indomethacin binds the Fe2+/Fe3+ ion. This was confirmed by a study using UV/Vis spectrophotometry. The results imply that indomethacin provides a neuroprotective effect by binding to iron and thus making it unavailable for free radical production.
- Full Text:
- Date Issued: 2003
- Authors: Anoopkumar-Dukie, Shailendra , Lack, Barbara , McPhail, Kerry L , Nyokong, Tebello , Lambat, Zaynab , Maharaj, Deepat , Daya, Santy
- Date: 2003
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/304763 , vital:58487 , xlink:href="https://doi.org/10.1023/A:1021958016928"
- Description: One of the hallmarks of Alzheimer's disease (AD) is the progressive degeneration of cholinergic neurons in the cerebral cortex and hippocampus. It is generally accepted that this neuronal degeneration is due to free-radical-induced damage. These free radicals attack vital structural components of the neurons. This implies that agents that reduce free radical generation could potentially delay the progression of AD. Free radical generation in the brain is assisted by the presence of iron, required by the Fenton reaction. Thus, agents that reduce iron availability for this reaction could potentially reduce free radical formation. Since non steroidal anti-inflammatory drugs (NSAIDS) have been shown to reduce the severity of AD, we investigated the possible mechanism by which indomethacin could afford neuroprotection. Our results show that indomethacin (1 mM) is able to reduce the iron-induced rise in lipid peroxidation in rat brain homogenates. In addition, our NMR data indicate that indomethacin binds the Fe2+/Fe3+ ion. This was confirmed by a study using UV/Vis spectrophotometry. The results imply that indomethacin provides a neuroprotective effect by binding to iron and thus making it unavailable for free radical production.
- Full Text:
- Date Issued: 2003
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
Interaction of serotonin and melatonin with sodium, potassium, calcium, lithium and aluminium
- Lack, Barbara, Daya, Santy, Nyokong, Tebello
- Authors: Lack, Barbara , Daya, Santy , Nyokong, Tebello
- Date: 2001
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/291553 , vital:56886 , xlink:href="https://doi.org/10.1034/j.1600-079x.2001.310202.x"
- Description: In the present study, we investigated the ability of serotonin and melatonin to bind metals that occur naturally in the brain. An electrochemical technique called adsorptive cathodic stripping voltammetry (AdCSV) was employed to study the metal–serotonin or metal–melatonin interactions. The results show that both serotonin and melatonin form stable complexes with lithium and potassium, with serotonin favouring lithium over potassium, and melatonin favouring potassium over lithium. Coordination between either serotonin or melatonin and calcium was not favoured. The stability of the complexes formed between serotonin and the metals decreased with the metals as follows: Li+>K+>Al3+>Na+>Ca2+. The trend for melatonin–metal complexes was K+>Li+>Na+>Al3+>Ca2+. The binding and stable complex formation between both ligands, serotonin and melatonin with lithium, potassium and sodium is of biological importance. The binding of serotonin to lithium could provide an explanation for the therapeutic effects of lithium in depression treatment, whereas the binding of aluminium by melatonin could provide insight into the role of this element in the aetiology of Alzheimer's disease.
- Full Text:
- Date Issued: 2001
- Authors: Lack, Barbara , Daya, Santy , Nyokong, Tebello
- Date: 2001
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/291553 , vital:56886 , xlink:href="https://doi.org/10.1034/j.1600-079x.2001.310202.x"
- Description: In the present study, we investigated the ability of serotonin and melatonin to bind metals that occur naturally in the brain. An electrochemical technique called adsorptive cathodic stripping voltammetry (AdCSV) was employed to study the metal–serotonin or metal–melatonin interactions. The results show that both serotonin and melatonin form stable complexes with lithium and potassium, with serotonin favouring lithium over potassium, and melatonin favouring potassium over lithium. Coordination between either serotonin or melatonin and calcium was not favoured. The stability of the complexes formed between serotonin and the metals decreased with the metals as follows: Li+>K+>Al3+>Na+>Ca2+. The trend for melatonin–metal complexes was K+>Li+>Na+>Al3+>Ca2+. The binding and stable complex formation between both ligands, serotonin and melatonin with lithium, potassium and sodium is of biological importance. The binding of serotonin to lithium could provide an explanation for the therapeutic effects of lithium in depression treatment, whereas the binding of aluminium by melatonin could provide insight into the role of this element in the aetiology of Alzheimer's disease.
- Full Text:
- Date Issued: 2001
Interaction of the neurotransmitter acetylcholine with aluminium, calcium and sodium
- Matlaba, Pulane M, Daya, Santy, Nyokong, Tebello
- Authors: Matlaba, Pulane M , Daya, Santy , Nyokong, Tebello
- Date: 2000
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/293246 , vital:57068 , xlink:href="https://doi.org/10.1211/146080800128735890"
- Description: Binding of aluminium to acetylcholine has important biological implications particularly in Alzheimer's disease. An electrochemical technique, adsorptive cathodic stripping voltammetry, has been employed in this study to investigate the in-situ formation of a complex between aluminium and acetylcholine. The stability of the resulting complex was compared with that of the in-situ complexes formed between acetylcholine and sodium or calcium. From the shifts in the reduction potential of the metals on addition of acetylcholine it is concluded that a strong complex is formed between acetylcholine and aluminium. Much weaker complexes are formed between calcium or sodium and acetylcholine. These results have important implications in the aetiology of Alzheimer's disease-in which brain aluminium concentrations are known to be high and brain cholinergic function is lower than normal.
- Full Text:
- Date Issued: 2000
- Authors: Matlaba, Pulane M , Daya, Santy , Nyokong, Tebello
- Date: 2000
- Subjects: To be catalogued
- Language: English
- Type: text , article
- Identifier: http://hdl.handle.net/10962/293246 , vital:57068 , xlink:href="https://doi.org/10.1211/146080800128735890"
- Description: Binding of aluminium to acetylcholine has important biological implications particularly in Alzheimer's disease. An electrochemical technique, adsorptive cathodic stripping voltammetry, has been employed in this study to investigate the in-situ formation of a complex between aluminium and acetylcholine. The stability of the resulting complex was compared with that of the in-situ complexes formed between acetylcholine and sodium or calcium. From the shifts in the reduction potential of the metals on addition of acetylcholine it is concluded that a strong complex is formed between acetylcholine and aluminium. Much weaker complexes are formed between calcium or sodium and acetylcholine. These results have important implications in the aetiology of Alzheimer's disease-in which brain aluminium concentrations are known to be high and brain cholinergic function is lower than normal.
- Full Text:
- Date Issued: 2000
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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