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Volume 12 (2019): Edizione 4 (December 2019)

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Volume 12 (2019): Edizione 1 (September 2019)

Volume 11 (2018): Edizione 4 (December 2018)

Volume 11 (2018): Edizione 3 (October 2018)

Volume 11 (2018): Edizione 2 (August 2018)

Volume 11 (2018): Edizione 1 (May 2018)

Volume 10 (2017): Edizione 4 (December 2017)

Volume 10 (2017): Edizione 3 (November 2017)

Volume 10 (2017): Edizione 2 (October 2017)

Volume 10 (2017): Edizione 1 (September 2017)

Volume 9 (2016): Edizione 3-4 (December 2016)

Volume 9 (2016): Edizione 2 (June 2016)

Volume 9 (2016): Edizione 1 (March 2016)

Volume 8 (2015): Edizione 4 (December 2015)

Volume 8 (2015): Edizione 3 (September 2015)

Volume 8 (2015): Edizione 2 (June 2015)

Volume 8 (2015): Edizione 1 (March 2015)

Volume 7 (2014): Edizione 4 (December 2014)

Volume 7 (2014): Edizione 3 (September 2014)

Volume 7 (2014): Edizione 2 (June 2014)

Volume 7 (2014): Edizione 1 (March 2014)

Volume 6 (2013): Edizione 4 (December 2013)

Volume 6 (2013): Edizione 3 (September 2013)

Volume 6 (2013): Edizione 2 (June 2013)

Volume 6 (2013): Edizione 1 (March 2013)

Volume 5 (2012): Edizione 4 (December 2012)

Volume 5 (2012): Edizione 3 (September 2012)

Volume 5 (2012): Edizione 2 (June 2012)

Volume 5 (2012): Edizione 1 (March 2012)

Volume 4 (2011): Edizione 4 (December 2011)

Volume 4 (2011): Edizione 3 (September 2011)

Volume 4 (2011): Edizione 2 (June 2011)

Volume 4 (2011): Edizione 1 (March 2011)

Volume 3 (2010): Edizione 4 (December 2010)

Volume 3 (2010): Edizione 3 (September 2010)

Volume 3 (2010): Edizione 2 (June 2010)

Volume 3 (2010): Edizione 1 (March 2010)

Volume 2 (2009): Edizione 4 (December 2009)

Volume 2 (2009): Edizione 3 (September 2009)

Volume 2 (2009): Edizione 2 (June 2009)

Volume 2 (2009): Edizione 1 (March 2009)

Volume 1 (2008): Edizione 3-4 (December 2008)

Volume 1 (2008): Edizione 2 (September 2008)

Volume 1 (2008): Edizione 1 (June 2008)

Dettagli della rivista
Formato
Rivista
eISSN
1337-9569
Pubblicato per la prima volta
19 Jun 2009
Periodo di pubblicazione
4 volte all'anno
Lingue
Inglese

Cerca

Volume 9 (2016): Edizione 2 (June 2016)

Dettagli della rivista
Formato
Rivista
eISSN
1337-9569
Pubblicato per la prima volta
19 Jun 2009
Periodo di pubblicazione
4 volte all'anno
Lingue
Inglese

Cerca

4 Articoli
Accesso libero

Review article. Predicting disease onset in clinically healthy people

Pubblicato online: 17 May 2017
Pagine: 39 - 54

Astratto

Abstract

Virtually all human disease is induced by oxidative stress. Oxidative stress, which is caused by toxic environmental exposure, the presence of disease, lifestyle choices, stress, chronic inflammation or combinations of these, is responsible for most disease. Oxidative stress from all sources is additive and it is the total oxidative stress from all sources that induces the onset of most disease. Oxidative stress leads to lipid peroxidation, which in turn produces Malondialdehyde. Serum malondialdehyde level is an additive parameter resulting from all sources of oxidative stress and, therefore, is a reliable indicator of total oxidative stress which can be used to predict the onset of disease in clinically asymptomatic individuals and to suggest the need for treatment that can prevent much human disease.

Parole chiave

  • disease prediction
  • disease prevention
  • disease mechanism
  • environmental disease
  • infectious disease
Accesso libero

Review article. Adverse hematological effects of hexavalent chromium: an overview

Pubblicato online: 17 May 2017
Pagine: 55 - 65

Astratto

Abstract

Workers of tanneries, welding industries, factories manufacturing chromate containing paints are exposed to hexavalent chromium that increas¬es the risk of developing serious adverse health effects. This review elucidates the mode of action of hexavalent chromium on blood and its adverse effects. Both leukocyte and erythrocyte counts of blood sharply decreased in Swiss mice after two weeks of intraperitoneal treatment with Cr (VI), with the erythrocytes transforming into echinocytes. The hexavalent chromium in the blood is readily reduced to trivalent form and the reductive capacity of erythrocytes is much greater than that of plasma. Excess Cr (VI), not reduced in plasma, may enter erythrocytes and lymphocytes and in rodents it induces microcytic anemia. The toxic effects of chromium (VI) include mitochondrial injury and DNA damage of blood cells that leads to carcinogenicity. Excess Cr (VI) increases cytosolic Ca2+ activity and ATP depletion thereby inducing eryptosis. Se, vitamin C, and quercetin are assumed to have some protective effect against hexavalent chromium induced hematological disorders.

Parole chiave

  • hexavalent chromium
  • haematological disorders
  • haemolytic anaemia
  • chromium in blood
Accesso libero

Original article. Mitigation of diazinon-induced cardiovascular and renal dysfunction by gallic acid

Pubblicato online: 17 May 2017
Pagine: 66 - 77

Astratto

Abstract

Studies of the link between environmental pollutants and cardiovascular dysfunction, neglected for decades, have recently provided new insights into the pathology and consequences of these killers. In this study, rats were divided into four groups, each containing 10 rats. The rats in group one served as controls and were administered normal saline, whereas the rats in group two were orally gavaged with 3 mg/kg of diazinon (DZN) alone for twenty one consecutive days. The rats in groups 3 and 4 were administered respective 60 mg/kg and 120 mg/kg gallic acid (GA) in addition to DZN for twenty one consecutive days. Exposure of rats to diazinon significantly (p<0.05) reduced the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) content. Malondialdehyde, hydrogen peroxide (H2O2) and nitric oxide (NO) contents were also significantly (p<0.05) elevated following DZN exposure. DZN further caused a significant (p<0.05) decrease of heart rate and QT interval prolongation. Hematologic analysis revealed significant reduction (p<0.05) in packed cell volume (PCV), hemoglobin concentration (Hb), red blood cell (RBC) count, and total white blood cell count of rats administered only DZN. Observations in this study suggest a modulatory role of gallic acid in diazinon-induced anemia and associated cardiovascular dysfunction in rats. Treatment with gallic acid reversed the oxidative stress markers studied, increased the antioxidant defence system and reduced deleterious effects on hematological parameters in rats. Pathologic findings of the heart and kidney were also found to be lessened.

Parole chiave

  • diazinon
  • gallic acid
  • heart
  • kidney
  • oxidative stress
  • cardiovascular dysfunction
Accesso libero

Original article. Protective effect of resveratrol against neuronal damage through oxidative stress in cerebral hemisphere of aluminum and fluoride treated rats

Pubblicato online: 17 May 2017
Pagine: 78 - 82

Astratto

Abstract

Aluminum has no defined biological function and it is potentially involved in the pathogenesis of neurodegenerative disorders. Furthermore, the presence of fluoride causes more aluminum to accumulate in the brain, resulting in increased neuronal damage. In recent years, resveratrol through its ameliorative effects was found to be a neuroprotectant. This study reports the protective effects of resveratrol on combined aluminum and fluoride induced neuronal damage through oxidative stress in rats. Protective effects of resveratrol (30 mg/kg b.w) on markers of oxidative stress were determined in rats exposed to aluminum chloride (100 mg/kg b.w) along with sodium fluoride (10 mg/kg b.w) for 8 weeks. The results showed a statistically significant (p<0.05) increase in lipid peroxidation (LPx) as well as a significant (p<0.05) decrease in superoxide dismutase and catalase activity. Enlarged cells, neurofibrillary tangles, and vacuolar spaces showing oxidative stress in the cerebral cortex were also observed in hematoxylin and eosin stained sections in aluminum and fluoride treated rats. Administration of resveratrol along with aluminum + fluoride showed significant reversal of oxidative stress and neuronal damage in rats. Thus resveratrol potentially acts as a neuroprotectant against aluminum chloride + sodium fluoride induced neuronal damage through its anti-oxidant efficacy.

Parole chiave

  • resveratrol
  • aluminium
  • fluoride
  • oxidative stress
  • neurodegeneration
4 Articoli
Accesso libero

Review article. Predicting disease onset in clinically healthy people

Pubblicato online: 17 May 2017
Pagine: 39 - 54

Astratto

Abstract

Virtually all human disease is induced by oxidative stress. Oxidative stress, which is caused by toxic environmental exposure, the presence of disease, lifestyle choices, stress, chronic inflammation or combinations of these, is responsible for most disease. Oxidative stress from all sources is additive and it is the total oxidative stress from all sources that induces the onset of most disease. Oxidative stress leads to lipid peroxidation, which in turn produces Malondialdehyde. Serum malondialdehyde level is an additive parameter resulting from all sources of oxidative stress and, therefore, is a reliable indicator of total oxidative stress which can be used to predict the onset of disease in clinically asymptomatic individuals and to suggest the need for treatment that can prevent much human disease.

Parole chiave

  • disease prediction
  • disease prevention
  • disease mechanism
  • environmental disease
  • infectious disease
Accesso libero

Review article. Adverse hematological effects of hexavalent chromium: an overview

Pubblicato online: 17 May 2017
Pagine: 55 - 65

Astratto

Abstract

Workers of tanneries, welding industries, factories manufacturing chromate containing paints are exposed to hexavalent chromium that increas¬es the risk of developing serious adverse health effects. This review elucidates the mode of action of hexavalent chromium on blood and its adverse effects. Both leukocyte and erythrocyte counts of blood sharply decreased in Swiss mice after two weeks of intraperitoneal treatment with Cr (VI), with the erythrocytes transforming into echinocytes. The hexavalent chromium in the blood is readily reduced to trivalent form and the reductive capacity of erythrocytes is much greater than that of plasma. Excess Cr (VI), not reduced in plasma, may enter erythrocytes and lymphocytes and in rodents it induces microcytic anemia. The toxic effects of chromium (VI) include mitochondrial injury and DNA damage of blood cells that leads to carcinogenicity. Excess Cr (VI) increases cytosolic Ca2+ activity and ATP depletion thereby inducing eryptosis. Se, vitamin C, and quercetin are assumed to have some protective effect against hexavalent chromium induced hematological disorders.

Parole chiave

  • hexavalent chromium
  • haematological disorders
  • haemolytic anaemia
  • chromium in blood
Accesso libero

Original article. Mitigation of diazinon-induced cardiovascular and renal dysfunction by gallic acid

Pubblicato online: 17 May 2017
Pagine: 66 - 77

Astratto

Abstract

Studies of the link between environmental pollutants and cardiovascular dysfunction, neglected for decades, have recently provided new insights into the pathology and consequences of these killers. In this study, rats were divided into four groups, each containing 10 rats. The rats in group one served as controls and were administered normal saline, whereas the rats in group two were orally gavaged with 3 mg/kg of diazinon (DZN) alone for twenty one consecutive days. The rats in groups 3 and 4 were administered respective 60 mg/kg and 120 mg/kg gallic acid (GA) in addition to DZN for twenty one consecutive days. Exposure of rats to diazinon significantly (p<0.05) reduced the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST) and reduced glutathione (GSH) content. Malondialdehyde, hydrogen peroxide (H2O2) and nitric oxide (NO) contents were also significantly (p<0.05) elevated following DZN exposure. DZN further caused a significant (p<0.05) decrease of heart rate and QT interval prolongation. Hematologic analysis revealed significant reduction (p<0.05) in packed cell volume (PCV), hemoglobin concentration (Hb), red blood cell (RBC) count, and total white blood cell count of rats administered only DZN. Observations in this study suggest a modulatory role of gallic acid in diazinon-induced anemia and associated cardiovascular dysfunction in rats. Treatment with gallic acid reversed the oxidative stress markers studied, increased the antioxidant defence system and reduced deleterious effects on hematological parameters in rats. Pathologic findings of the heart and kidney were also found to be lessened.

Parole chiave

  • diazinon
  • gallic acid
  • heart
  • kidney
  • oxidative stress
  • cardiovascular dysfunction
Accesso libero

Original article. Protective effect of resveratrol against neuronal damage through oxidative stress in cerebral hemisphere of aluminum and fluoride treated rats

Pubblicato online: 17 May 2017
Pagine: 78 - 82

Astratto

Abstract

Aluminum has no defined biological function and it is potentially involved in the pathogenesis of neurodegenerative disorders. Furthermore, the presence of fluoride causes more aluminum to accumulate in the brain, resulting in increased neuronal damage. In recent years, resveratrol through its ameliorative effects was found to be a neuroprotectant. This study reports the protective effects of resveratrol on combined aluminum and fluoride induced neuronal damage through oxidative stress in rats. Protective effects of resveratrol (30 mg/kg b.w) on markers of oxidative stress were determined in rats exposed to aluminum chloride (100 mg/kg b.w) along with sodium fluoride (10 mg/kg b.w) for 8 weeks. The results showed a statistically significant (p<0.05) increase in lipid peroxidation (LPx) as well as a significant (p<0.05) decrease in superoxide dismutase and catalase activity. Enlarged cells, neurofibrillary tangles, and vacuolar spaces showing oxidative stress in the cerebral cortex were also observed in hematoxylin and eosin stained sections in aluminum and fluoride treated rats. Administration of resveratrol along with aluminum + fluoride showed significant reversal of oxidative stress and neuronal damage in rats. Thus resveratrol potentially acts as a neuroprotectant against aluminum chloride + sodium fluoride induced neuronal damage through its anti-oxidant efficacy.

Parole chiave

  • resveratrol
  • aluminium
  • fluoride
  • oxidative stress
  • neurodegeneration

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