Impact of Lead Toxicity on Brain Metabolisms of Nucleic Acid and Catecholamine in Protein Malnourished Rats.

Ghosh, Susmita; Chatterjee, Ankit; Gupta, Malaya

doi:10.3177/jnsv.38.451

Cited by 17 publications

(1 citation statement)

References 39 publications

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“…En 1992, Gerhard [3] a rapporté qu'une déficience en Ca 2+ augmente les perturbations induites par les métaux lourds. Chosh [4] a observé que les effets du Pb au niveau du système nerveux étaient aggravés chez des rats mal nourris. Newberne [5] a montré également que l'exposition au Ni de rats adultes souffrant d'une déficience minérale surtout en Mg amplifie le taux des maladies rénales.…”

Section: Introductionunclassified

Interaction du jeûne intermittent sur les effets cytotoxiques rénaux du nickel chez le rat pubère

Hfaïedh

Allaqui

Croute³

et al. 2005

Comptes Rendus. Biologies

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zone corticale, les capsules de Bowman adhérant aux glomérules, et ceci aux dépens des espaces des chambres glomérulaires qui diminuent beaucoup au niveau du tube proximal. On note une vacuolisation et une hypertrophie des cellules épithéliales, et ceci au dépend de l'interstitium rénal et des vaisseaux, qui se trouvent comprimés, ce qui rendrait difficile les fonctions rénales de filtration et de sécrétion tubulaire. L'association du jeûne intermittent avec le nickel inhibe cette défaillance rénale. Le dosage de la protéine de stress Hsp72 et des métallothionéines (MT) montre que le nickel induit une baisse de l'expression de la Hsp72 et de la synthèse des MT au niveau des tissus rénaux. Cependant la diminution de ces deux biomarqueurs (Hsp72 et MT) est plus faible dans le cas où le nickel est associé au jeûne intermittent (groupe JNi). En conclusion, le jeûne intermittent n'induit pas une déficience minérale. Il ne peut pas être considéré donc comme une malnutrition. Il s'agit plutôt d'une restriction calorique bénéfique pour l'organisme en augmentant ses performances face à l'intoxication au nickel.

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Section: Introductionunclassified

Interaction du jeûne intermittent sur les effets cytotoxiques rénaux du nickel chez le rat pubère

Hfaïedh

Allaqui

Croute³

et al. 2005

Comptes Rendus. Biologies

View full text Add to dashboard Cite

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?-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure

Chang

Tsao

et al. 2004

Arch Toxicol

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To understanding the reversible or irreversible harm to the beta-adrenergic system in the brain of lead-exposed rats, this study sets up an animal model to estimate the change in the sympathetic nervous system of brain after lead exposure was withdrawn. We address the following topics in this study: (a) the relationship between withdrawal time of lead exposure and brain beta-adrenergic receptor, blood lead level, and brain lead level in lead-exposed rats after lead exposure was stopped; and (b) the relationship between lead level and beta-adrenergic receptor and cyclic AMP (c-AMP) in brain. Wistar rats were chronically fed with 2% lead acetate and water for 2 months. Radioligand binding was assayed by a method that fulfilled strict criteria of beta-adrenergic receptor using the ligand [125I]iodocyanopindolol. The levels of lead were determined by electrothermal atomic absorption spectrometry. The c-AMP level was determined by radioimmunoassay. The results showed a close relationship between decreasing lead levels and increasing numbers of brain beta-adrenergic receptors and brain adenylate cyclase activity after lead exposure was withdrawn. The effect of lead exposure on the beta-adrenergic system of the brain is a partly reversible condition.

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Lead (Pb), a threat to protein metabolic efficacy of liver, kidney and muscle in mice

Das

Pal

2017

Comp Clin Pathol

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Lead, being the most dangerous natural heavy metal imposes metabolic dysfunction in organ system. However, the effect of lead on protein metabolic efficacy in the liver, kidney and skeletal muscle in mice has not been well studied. The aim of the present study is to establish the metabolic orientation between the liver, kidney and muscle upon subacute lead exposure to assess how protein and amino acid metabolisms are affected. Lead acetate was administered by gavage at a dose of 5 mg/kg b.w./once daily for 30 days. After the treatment, the liver, kidney and muscle were evaluated for biochemical parameters such as proteolytic enzyme activities (trypsin, cathepsin and pronase), tissue protein content (acidic, basic, neutral and total protein), protein carbonyl content, free amino nitrogen as well as tissue and serum transaminase activities. Degradation of total protein was noted in the liver and kidney possibly due to enhanced carbonylation of proteins whereas it was elevated in skeletal muscle. The proteolytic enzyme activity was inhibited in the liver and elevated in the kidney by lead treatment. Muscular cathepsin and trypsin activities decreased but the pronase activity enhanced following lead exposure. Moreover, a marked reduction of transaminase enzyme activities in all the tissues might be due to enzyme leakage from tissue to blood. Significant alteration in amino acid nitrogen in the affected tissue indicates adaptive mechanisms at play in the organ system. Lead is found to be responsible for alteration of tissue protein and amino acids in a toxic fashion and promotes a cooperative mechanism to minimize the metabolic distress imposed by lead.

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Impact of Lead Toxicity on Brain Metabolisms of Nucleic Acid and Catecholamine in Protein Malnourished Rats.

Cited by 17 publications

References 39 publications

Interaction du jeûne intermittent sur les effets cytotoxiques rénaux du nickel chez le rat pubère

Interaction du jeûne intermittent sur les effets cytotoxiques rénaux du nickel chez le rat pubère

?-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure

Lead (Pb), a threat to protein metabolic efficacy of liver, kidney and muscle in mice

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