The interrelationship between gasotransmitters and lead-induced renal toxicity in rats

Abdel-Zaher, Ahmed O.; Abd-ellatief, Rasha B.; Aboulhagag, Noha A.; Farghaly, Hanan S.M.; AL-Wasei, Fahmy M.M.

doi:10.1016/j.toxlet.2019.04.012

“…These pathological alterations may include increased oxidative stress [9], neurological deficits [39], decreased motor coordination, and cognitive deficits [40,41]. Alterations in astrocyte maturation, degeneration of neural cells [39,41], renal dysfunction, degenerative changes in tubular epithelium, and hepatotoxicity [2,42] were also reported in Pb poisoning, both in humans and different rodent species. In the present study, a rat model was used to investigate the therapeutic potentials of curcumin on the fundamental mechanisms of motor dysfunction and neurodegeneration caused by Pb toxicity.…”

Section: Discussionmentioning

confidence: 99%

“…Lead (Pb) is a ubiquitous environmental neurotoxin that induces several physiological, behavioral, and biochemical abnormalities in humans and animals [1]. Pb toxicity remains a common problem in both developing and industrialized countries due to unavoidable environmental and occupational exposure, resulting in about 600,000 new cases of intellectual disabilities in children and 143,000 deaths per year [1,2]. Although data from the Adults Blood Lead Epidemiology and Surveillance (ABLES) program indicate a significant decrease in the incidence of blood lead levels (BLLs) among adult industrial workers, occupational exposure to Pb remains a public health concern, accounting for about 94% of Pb exposure [3].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Chelating Activity and Inhibition of Oxidative Stress

Abubakar

¹

,

Mailafiya

²

,

Danmaigoro

³

et al. 2019

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Lead (Pb) is a toxic, environmental heavy metal that induces serious clinical defects in all organs, with the nervous system being its primary target. Curcumin is the main active constituent of turmeric rhizome (Curcuma longa) with strong antioxidant and anti-inflammatory properties. This study is aimed at evaluating the therapeutic potentials of curcumin on Pb-induced neurotoxicity. Thirty-six male Sprague Dawley rats were randomly assigned into five groups with 12 rats in the control (normal saline) and 6 rats in each of groups, i.e., the lead-treated group (LTG) (50 mg/kg lead acetate for four weeks), recovery group (RC) (50 mg/kg lead acetate for four weeks), treatment group 1 (Cur100) (50 mg/kg lead acetate for four weeks, followed by 100 mg/kg curcumin for four weeks) and treatment group 2 (Cur200) (50 mg/kg lead acetate for four weeks, followed by 200 mg/kg curcumin for four weeks). All experimental groups received oral treatment via orogastric tube on alternate days. Motor function was assessed using a horizontal bar method. The cerebellar concentration of Pb was evaluated using ICP-MS technique. Pb-administered rats showed a significant decrease in motor scores and Superoxide Dismutase (SOD) activity with increased Malondialdehyde (MDA) levels. In addition, a marked increase in cerebellar Pb concentration and alterations in the histological architecture of the cerebellar cortex layers were recorded. However, treatment with curcumin improved the motor score, reduced Pb concentration in the cerebellum, and ameliorated the markers of oxidative stress, as well as restored the histological architecture of the cerebellum. The results of this study suggest that curcumin attenuates Pb-induced neurotoxicity via inhibition of oxidative stress and chelating activity.

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“…These pathological alterations may include increase oxidative stress [9], neurological deficit [21], decrease motor coordination and cognitive deficit [22,23]. Alteration in astrocyte maturation, degeneration of neural cells [21,23], renal dysfunction, degenerative changes in tubular epithelium and hepatotoxicity [2,24] were also reported in Pb poisoning both in humans and different rodents species. In the present study, rat that is vulnerable to intoxication and poisoning with the cerebellar circuit especially the purkinje cells susceptible to injury after exposure to environmental toxins such as Pb [30].…”

Section: Discussionmentioning

confidence: 99%

“…Lead (Pb) is a ubiquitous environmental neurotoxin that induces several physiological, behavioral and biochemical abnormalities in humans and animals [1]. Pb toxicity remain a common problem in both developing and industrialized countries due to unavoidable environmental and occupational exposure resulting to about 600,000 new cases of intellectual disabilities in children and account for about 143,000 deaths per year [1,2]. Although data from Adults Blood Lead Epidemiology and Surveillance (ABLES) program indicates a significant decrease in incidence of blood lead levels (BLLs) among adults' industrial workers, occupational exposure Pb remained a public health concern accounting for about 94% Pb exposures [3].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Inhibition of Oxidative Stress and Chelating Activity

Abubakar¹,

Mailafiya²,

Danmaigoro³

et al. 2019

Preprint

View full text Add to dashboard Cite

Lead (Pb) is a toxic environmental heavy metal that induces serious clinical defect on all organs with the nervous system being the primary target. Curcumin is the main active constituent of turmeric rhizome (Curcuma longa) with strong antioxidant and anti-inflammatory properties. This study is aimed at evaluating the therapeutic potentials of curcumin on Pb-induced neurotoxicity. Thirty six male Sprague Dawley rats were randomly assigned into five (5) groups with 12 rats in the control (normal saline) and 6 rats for the lead treated group (LTG) (50 mg/kg lead acetate for 4 weeks), recovery group (RC) (50 mg/kg lead acetate for 4 weeks), treatment group 1 (Cur100) (50 mg/kg lead acetate for 4 weeks, followed by 100 mg/kg curcumin for 4 weeks) and treatment group 2 (Cur200) (50 mg/kg lead acetate for 4 weeks, followed by 200 mg/kg curcumin for 4 weeks) groups each. All experimental groups received the oral treatments through orogastric-tube on alternate days. Motor function was assessed using horizontal bar method while Pb concentration in the cerebellum of the rats were evaluated using ICP-MS techniques. Pb-administered rats showed significant decrease in motor scores, SOD activity with increase MDA levels and Pb concentration in their cerebellum with marked alterations in the histological architecture of the cerebellar cortex layers. However, treatment with curcumin improved the motor score, reduced Pb concentration in the cerebellum and ameliorates the markers of oxidative stress as well as restored the histological architecture of the cerebellum. The results this in study suggested that curcumin attenuates Pb-induced neurotoxicity via inhibition of oxidative stress and chelating activity.

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“…These pathological alterations may include increase oxidative stress [9], neurological deficit [28], decrease motor coordination and cognitive deficit [29,30]. Alteration in astrocyte maturation, degeneration of neural cells [28,30], renal dysfunction, degenerative changes in tubular epithelium and hepatotoxicity [2,31] were also reported in Pb poisoning both in humans and different rodents species. In the present study, rat model of Pb toxicity was used to investigate the therapeutic potentials of curcumin on fundamental mechanism of motor Worthy to note in this study, is the choice of male Sprague Dawley rats for all the experimentations.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Inhibition of Oxidative Stress and Chelating Activity

Abubakar¹,

Mm²,

Danmaigoro³

et al. 2019

Preprint

View full text Add to dashboard Cite

Lead (Pb) is a toxic environmental heavy metal that induces serious clinical defect on all organs with the nervous system being the primary target. Curcumin is the main active constituent of turmeric rhizome (Curcuma longa) with strong antioxidant and anti-inflammatory properties. This study is aimed at evaluating the therapeutic potentials of curcumin on Pb-induced neurotoxicity. Thirty six male Sprague Dawley rats were randomly assigned into five (5) groups with 12 rats in the control (normal saline) and 6 rats for the lead treated group (LTG) (50 mg/kg lead acetate for 4 weeks), recovery group (RC) (50 mg/kg lead acetate for 4 weeks), treatment group 1 (Cur100) (50 mg/kg lead acetate for 4 weeks, followed by 100 mg/kg curcumin for 4 weeks) and treatment group 2 (Cur200) (50 mg/kg lead acetate for 4 weeks, followed by 200 mg/kg curcumin for 4 weeks) groups each. All experimental groups received the oral treatments through orogastric-tube on alternate days. Motor function was assessed using horizontal bar method while Pb concentration in the cerebellum of the rats were evaluated using ICP-MS techniques. Pb-administered rats showed significant decrease in motor scores, SOD activity with increase MDA levels and Pb concentration in their cerebellum with marked alterations in the histological architecture of the cerebellar cortex layers. However, treatment with curcumin improved the motor score, reduced Pb concentration in the cerebellum and ameliorates the markers of oxidative stress as well as restored the histological architecture of the cerebellum. The results this in study suggested that curcumin attenuates Pb-induced neurotoxicity via inhibition of oxidative stress and chelating activity.

show abstract

The interrelationship between gasotransmitters and lead-induced renal toxicity in rats

Cited by 24 publications

References 46 publications

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Chelating Activity and Inhibition of Oxidative Stress

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Chelating Activity and Inhibition of Oxidative Stress

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Inhibition of Oxidative Stress and Chelating Activity

Curcumin Attenuates Lead-Induced Cerebellar Toxicity in Rats via Inhibition of Oxidative Stress and Chelating Activity

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