Rivista e Edizione

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 10 (2017): Edizione 1 (September 2017)

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

6 Articoli

Original Article

Accesso libero

Protective efficacy of various carbonyl compounds and their metabolites, and nutrients against acute toxicity of some cyanogens in rats: biochemical and physiological studies

Pubblicato online: 14 Feb 2018
Pagine: 1 - 10

Astratto

Abstract

Cyanogens are widely used in industries and their toxicity is mainly due to cyanogenesis. The antidotes for cyanide are usually instituted for the management of cyanogen poisoning. The present study reports the protective efficacy of 14 carbonyl compounds and their metabolites, and nutrients (1.0 g/kg; oral; +5 min) against acute oral toxicity of acetonitrile (ATCN), acrylonitrile (ACN), malononitrile (MCN), propionitrile (PCN), sodium nitroprusside (SNP), succinonitrile (SCN), and potassium ferricyanide (PFCN) in rats. Maximum protection index was observed for alpha-ketoglutarate (A-KG) against MCN and PCN (5.60), followed by dihydroxyacetone (DHA) against MCN (2.79). Further, MCN (0.75 LD50) caused significant increase in cyanide concentration in brain, liver and kidney and inhibition of cytochrome c oxidase activity in brain and liver, which favorably responded to A-KG and DHA treatment. Up-regulation of inducible nitric oxide synthase by MCN, PCN and SNP, and uncoupling protein by PCN and SNP observed in the brain was abolished by A-KG administration. However, no DNA damage was detected in the brain. MCN and SNP significantly decreased the mean arterial pressure, heart rate, respiratory rate and neuromuscular transmission, which were resolved by A-KG. The study suggests a beneficial effect of A-KG in the treatment of acute cyanogen poisoning.

Parole chiave

  • cyanogens
  • cyanide
  • acute toxicity
  • protection
  • biochemistry
  • physiology
Accesso libero

Pyridoindole SMe1EC2 as cognition enhancer in ageing-related cognitive decline

Pubblicato online: 14 Feb 2018
Pagine: 11 - 19

Astratto

Abstract

Synthetic pyridoindole-type substances derived from the lead compound stobadine represent promising agents in treatment of a range of pathologies including neurological disorders. The beneficial biological effects were suggested to be likely associated with their capacity to ameliorate oxidative damage.

In our study, the effect of supplementation with the derivative of stobadine, SMe1EC2, on ageing-related cognitive decline in rats was investigated. The 20-months-old male Wistar rats were administered SMe1EC2 at a low dose, 0.5 mg/kg, daily during eight weeks. Morris water maze test was performed to assess the spatial memory performances. The cell-based assays of capacity of SMe1EC2 to modulate proinflammatory generation of oxidants by microglia were also performed.

The rats treated with SMe1EC2 showed significantly increased path efficiency, significantly shorter time interval of successful trials and exerted also notably lower frequencies of clockwise rotations in the pool compared to non-supplemented aged animals. Mildly improved parameters included test durations, distances to reach the platform, time in periphery of the pool and overall rotations in the water maze. However, the pyridoindole SMe1EC2 did not show profound inhibitory effect on production of nitric oxide and superoxide by activated microglial cells.

In conclusion, our study suggests that pyridoindole SMe1EC2, at low doses administered chronically, can act as cognition enhancing agent in aged rats. The protective mechanism less likely involves direct modulation of proinflammatory and prooxidant state of microglia, the prominent mediators of neurotoxicity in brain ageing and neurodegeneration.

Parole chiave

  • brain ageing
  • cognitive decline
  • antioxidants
  • pyridoindoles
Accesso libero

Melatonin protects against chromium (VI) induced hepatic oxidative stress and toxicity: Duration dependent study with realistic dosage

Pubblicato online: 14 Feb 2018
Pagine: 20 - 29

Astratto

Abstract

The present study was undertaken to assess the degree of oxidative stress and toxic effects induced by chromium on hepatic tissue in male Wistar rats exposed to a realistic dosage of Cr(VI) (20 mg/kg/b.w./day) through drinking water, based on the levels of these metals found in the environment, for a duration of 15, 30 and 60 days. The protective effect of melatonin (10 mg/kg) was also studied by simultaneous administration with the metal. Levels of enzymatic and non-enzymatic antioxidants as well as lipid peroxidation were assessed. There was a significant decrease in enzymatic as well as non-enzymatic antioxidants and an increase in the lipid peroxidation level, which were prevented and maintained at near-normal levels by the administration of melatonin in all treatment periods. Metal accumulation was maximal at 15 days, with gradual decreases till 60 days. Histopathological observations also demonstrated the fact that Cr (VI) exposure leads to cytological lesions in the hepatic tissue promoting cellular necrotic/apoptotic changes, while melatonin was able to counteract insults induced by Cr (VI) at all treatment periods. It also prevented alterations in insulin and glucose levels. Overall, the present study suggests a duration-dependent effect of Cr on hepatic oxidative stress and cytotoxicity and shows the potent activity of melatonin in preventing the negative effects of Cr (VI).

Parole chiave

  • melatonin
  • oxidative stress
  • toxicity, chromium (VI)

Minireview

Accesso libero

Risks of using SSRI / SNRI antidepressants during pregnancy and lactation

Pubblicato online: 14 Feb 2018
Pagine: 30 - 34

Astratto

Abstract

At present, affective disorders are among the most commonly diagnosed mental diseases. In pregnancy, they can occur as pre-delivery depression, recurrent depressive disorder or postnatal depression. The estimated prevalence of depressive disorders in pregnancy is approximately 9–16%, with some statistics reporting up to 20%. Approximately 2–3% of pregnant women take antidepressants during pregnancy, and the number of mothers treated increases by birth to 5–7%. Treatment of depression during pregnancy and breastfeeding is a controversial issue, as antidepressants can negatively affect the developing fetus. According to epidemiological studies, the effects of treated depression in pregnancy are related to premature birth, decreased body weight of the child, intrauterine growth retardation, neonatal adaptive syndrome, and persistent pulmonary hypertension. However, untreated depression can adversely affect maternal health and increase the risk of preeclampsia and eclampsia, as well as of subsequent postnatal depression, which can lead to disruption of the mother-child relationship. Based on the above mentioned facts, the basic question arises as to whether or not to treat depression during pregnancy and lactation.

Parole chiave

  • depression
  • antidepressants
  • pregnancy
  • lactation
  • fetus
  • brain
  • behavioral disorders
Accesso libero

Animal models of maternal depression for monitoring neurodevelopmental changes occurring in dams and offspring

Pubblicato online: 14 Feb 2018
Pagine: 35 - 39

Astratto

Abstract

Depression is one of the most prevalent and life-threatening forms of mental illness affecting about 20% of the population. Depressive disorder as a biochemical phenomenon, was first recognized in the mid-20th century of research, however the etiology of this disease is still not well understood. Although the need to investigate depressive disorders has emerged from the needs of clinical practice, there are many preclinical studies, which brought new insights into this field of research. During experimental work it was crucial to develop appropriate animal models, where the neurohumoral mechanism was similar to humans. In the past decades, several animal models of maternal depression have been developed. We describe the three most popular rodent models of maternal depression which are based on 1. stress prior to gestation, 2. prenatal stress and 3. early life stress. The above-mentioned animal models appear to fulfill many criteria for a relevant animal model of depression; they alter the regulation of the HPA, induce signs of depression-like behavior and several antidepressant treatments can reverse the state induced by maternal stress. Although, they are not able to model all aspects of maternal depression, they are useful models for monitoring neurodevelopmental changes occurring in dams and offspring.

Parole chiave

  • rat
  • animal model
  • depression
  • pregnancy

Short Communication

Accesso libero

Animal tests for anxiety-like and depression-like behavior in rats

Pubblicato online: 14 Feb 2018
Pagine: 40 - 43

Astratto

Abstract

An animal model of human behavior represents a complex of cognitive and/or emotional processess, which are translated from animals to humans. A behavioral test is developed primarily and specifically to verify and support a theory of cognition or emotion; it can also be used to verify a theory of a psychopathology, but it is not developed for a particular type of psychopathology. The paper reviews tests commonly used in novel drug discovery research. Focus is especially on tests which can evaluate anxiety-like (open-field test, novelty suppressed feeding, elevated plus maze, light/dark box, stressinduced hyperthermia) and depression-like behaviors (forced swim test, tail suspension test, sucrose preference test) as they represent an important methodological tool in pre-clinical as well as in behavioral toxicology studies.

Parole chiave

  • behavior
  • rat
  • anxiety
  • depression
  • tests
6 Articoli

Original Article

Accesso libero

Protective efficacy of various carbonyl compounds and their metabolites, and nutrients against acute toxicity of some cyanogens in rats: biochemical and physiological studies

Pubblicato online: 14 Feb 2018
Pagine: 1 - 10

Astratto

Abstract

Cyanogens are widely used in industries and their toxicity is mainly due to cyanogenesis. The antidotes for cyanide are usually instituted for the management of cyanogen poisoning. The present study reports the protective efficacy of 14 carbonyl compounds and their metabolites, and nutrients (1.0 g/kg; oral; +5 min) against acute oral toxicity of acetonitrile (ATCN), acrylonitrile (ACN), malononitrile (MCN), propionitrile (PCN), sodium nitroprusside (SNP), succinonitrile (SCN), and potassium ferricyanide (PFCN) in rats. Maximum protection index was observed for alpha-ketoglutarate (A-KG) against MCN and PCN (5.60), followed by dihydroxyacetone (DHA) against MCN (2.79). Further, MCN (0.75 LD50) caused significant increase in cyanide concentration in brain, liver and kidney and inhibition of cytochrome c oxidase activity in brain and liver, which favorably responded to A-KG and DHA treatment. Up-regulation of inducible nitric oxide synthase by MCN, PCN and SNP, and uncoupling protein by PCN and SNP observed in the brain was abolished by A-KG administration. However, no DNA damage was detected in the brain. MCN and SNP significantly decreased the mean arterial pressure, heart rate, respiratory rate and neuromuscular transmission, which were resolved by A-KG. The study suggests a beneficial effect of A-KG in the treatment of acute cyanogen poisoning.

Parole chiave

  • cyanogens
  • cyanide
  • acute toxicity
  • protection
  • biochemistry
  • physiology
Accesso libero

Pyridoindole SMe1EC2 as cognition enhancer in ageing-related cognitive decline

Pubblicato online: 14 Feb 2018
Pagine: 11 - 19

Astratto

Abstract

Synthetic pyridoindole-type substances derived from the lead compound stobadine represent promising agents in treatment of a range of pathologies including neurological disorders. The beneficial biological effects were suggested to be likely associated with their capacity to ameliorate oxidative damage.

In our study, the effect of supplementation with the derivative of stobadine, SMe1EC2, on ageing-related cognitive decline in rats was investigated. The 20-months-old male Wistar rats were administered SMe1EC2 at a low dose, 0.5 mg/kg, daily during eight weeks. Morris water maze test was performed to assess the spatial memory performances. The cell-based assays of capacity of SMe1EC2 to modulate proinflammatory generation of oxidants by microglia were also performed.

The rats treated with SMe1EC2 showed significantly increased path efficiency, significantly shorter time interval of successful trials and exerted also notably lower frequencies of clockwise rotations in the pool compared to non-supplemented aged animals. Mildly improved parameters included test durations, distances to reach the platform, time in periphery of the pool and overall rotations in the water maze. However, the pyridoindole SMe1EC2 did not show profound inhibitory effect on production of nitric oxide and superoxide by activated microglial cells.

In conclusion, our study suggests that pyridoindole SMe1EC2, at low doses administered chronically, can act as cognition enhancing agent in aged rats. The protective mechanism less likely involves direct modulation of proinflammatory and prooxidant state of microglia, the prominent mediators of neurotoxicity in brain ageing and neurodegeneration.

Parole chiave

  • brain ageing
  • cognitive decline
  • antioxidants
  • pyridoindoles
Accesso libero

Melatonin protects against chromium (VI) induced hepatic oxidative stress and toxicity: Duration dependent study with realistic dosage

Pubblicato online: 14 Feb 2018
Pagine: 20 - 29

Astratto

Abstract

The present study was undertaken to assess the degree of oxidative stress and toxic effects induced by chromium on hepatic tissue in male Wistar rats exposed to a realistic dosage of Cr(VI) (20 mg/kg/b.w./day) through drinking water, based on the levels of these metals found in the environment, for a duration of 15, 30 and 60 days. The protective effect of melatonin (10 mg/kg) was also studied by simultaneous administration with the metal. Levels of enzymatic and non-enzymatic antioxidants as well as lipid peroxidation were assessed. There was a significant decrease in enzymatic as well as non-enzymatic antioxidants and an increase in the lipid peroxidation level, which were prevented and maintained at near-normal levels by the administration of melatonin in all treatment periods. Metal accumulation was maximal at 15 days, with gradual decreases till 60 days. Histopathological observations also demonstrated the fact that Cr (VI) exposure leads to cytological lesions in the hepatic tissue promoting cellular necrotic/apoptotic changes, while melatonin was able to counteract insults induced by Cr (VI) at all treatment periods. It also prevented alterations in insulin and glucose levels. Overall, the present study suggests a duration-dependent effect of Cr on hepatic oxidative stress and cytotoxicity and shows the potent activity of melatonin in preventing the negative effects of Cr (VI).

Parole chiave

  • melatonin
  • oxidative stress
  • toxicity, chromium (VI)

Minireview

Accesso libero

Risks of using SSRI / SNRI antidepressants during pregnancy and lactation

Pubblicato online: 14 Feb 2018
Pagine: 30 - 34

Astratto

Abstract

At present, affective disorders are among the most commonly diagnosed mental diseases. In pregnancy, they can occur as pre-delivery depression, recurrent depressive disorder or postnatal depression. The estimated prevalence of depressive disorders in pregnancy is approximately 9–16%, with some statistics reporting up to 20%. Approximately 2–3% of pregnant women take antidepressants during pregnancy, and the number of mothers treated increases by birth to 5–7%. Treatment of depression during pregnancy and breastfeeding is a controversial issue, as antidepressants can negatively affect the developing fetus. According to epidemiological studies, the effects of treated depression in pregnancy are related to premature birth, decreased body weight of the child, intrauterine growth retardation, neonatal adaptive syndrome, and persistent pulmonary hypertension. However, untreated depression can adversely affect maternal health and increase the risk of preeclampsia and eclampsia, as well as of subsequent postnatal depression, which can lead to disruption of the mother-child relationship. Based on the above mentioned facts, the basic question arises as to whether or not to treat depression during pregnancy and lactation.

Parole chiave

  • depression
  • antidepressants
  • pregnancy
  • lactation
  • fetus
  • brain
  • behavioral disorders
Accesso libero

Animal models of maternal depression for monitoring neurodevelopmental changes occurring in dams and offspring

Pubblicato online: 14 Feb 2018
Pagine: 35 - 39

Astratto

Abstract

Depression is one of the most prevalent and life-threatening forms of mental illness affecting about 20% of the population. Depressive disorder as a biochemical phenomenon, was first recognized in the mid-20th century of research, however the etiology of this disease is still not well understood. Although the need to investigate depressive disorders has emerged from the needs of clinical practice, there are many preclinical studies, which brought new insights into this field of research. During experimental work it was crucial to develop appropriate animal models, where the neurohumoral mechanism was similar to humans. In the past decades, several animal models of maternal depression have been developed. We describe the three most popular rodent models of maternal depression which are based on 1. stress prior to gestation, 2. prenatal stress and 3. early life stress. The above-mentioned animal models appear to fulfill many criteria for a relevant animal model of depression; they alter the regulation of the HPA, induce signs of depression-like behavior and several antidepressant treatments can reverse the state induced by maternal stress. Although, they are not able to model all aspects of maternal depression, they are useful models for monitoring neurodevelopmental changes occurring in dams and offspring.

Parole chiave

  • rat
  • animal model
  • depression
  • pregnancy

Short Communication

Accesso libero

Animal tests for anxiety-like and depression-like behavior in rats

Pubblicato online: 14 Feb 2018
Pagine: 40 - 43

Astratto

Abstract

An animal model of human behavior represents a complex of cognitive and/or emotional processess, which are translated from animals to humans. A behavioral test is developed primarily and specifically to verify and support a theory of cognition or emotion; it can also be used to verify a theory of a psychopathology, but it is not developed for a particular type of psychopathology. The paper reviews tests commonly used in novel drug discovery research. Focus is especially on tests which can evaluate anxiety-like (open-field test, novelty suppressed feeding, elevated plus maze, light/dark box, stressinduced hyperthermia) and depression-like behaviors (forced swim test, tail suspension test, sucrose preference test) as they represent an important methodological tool in pre-clinical as well as in behavioral toxicology studies.

Parole chiave

  • behavior
  • rat
  • anxiety
  • depression
  • tests

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