Zinc ameliorates lead toxicity by reducing body Pb burden and restoring Pb-induced haematological and biochemical derangements

Ugwuja, Emmanuel Ike; N, Vincent; Ikaraoha, Ikechukwu Chidiebere; Ohayi, Samuel Robsam

doi:10.1177/2397847320956562

Cited by 6 publications

(6 citation statements)

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“…Zinc supplementation has been suggested to partially minimize the Pb tissue uptake and mitigate against Pb-induced toxicity. However, the specific mechanisms by which this is achieved remain unclear [ 3 , 31 , 41 ]. Some authors indicate that the reduced tissue Pb uptake is due to the competitive interaction of Pb and Zn divalent ions at absorption sites in the gastrointestinal tract into systemic circulation and transportation into tissues [ 3 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…However, the specific mechanisms by which this is achieved remain unclear [ 3 , 31 , 41 ]. Some authors indicate that the reduced tissue Pb uptake is due to the competitive interaction of Pb and Zn divalent ions at absorption sites in the gastrointestinal tract into systemic circulation and transportation into tissues [ 3 , 41 ]. In our study, zinc supplementation was associated with reduced accumulation of Pb in testes and muscles at low exposure and an increased Pb accumulation at high exposure in both tissues.…”

Section: Discussionmentioning

confidence: 99%

“…In the present study, Pb-induced renal and hepatic toxicities were not pronounced as evidenced by lack of changes in primary biochemical parameters of the liver or kidney and related enzymes, plasma biochemistry, MDA and the total antioxidant capacity [ 41 ]. This suggests that the Pb tissue burden may not have been severe to elicit overt tissue damage.…”

Section: Discussionmentioning

confidence: 99%

“…Lead (Pb) is a widely recognized metal toxicant that persists in the environment and is known to induce several derangements in biochemical and physiological systems in humans and animals [ 42 ]. The most recognized biomarker of effect in Pb exposure is the impairment and inhibition of delta aminolaevulinic acid dehydratase (ALAD) enzyme activity that eventually affects heme synthesis with anemia as sequela [ 41 ]. Ingestion of dust or soil containing Pb through hand-to-mouth activities has been suggested as a major route of exposure in children [ 42 ].…”

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confidence: 99%

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Effects of zinc on tissue uptake and toxicity of lead in Sprague Dawley rat

et al. 2021

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Lead (Pb) exposure occurs together with other metals including zinc (Zn). This study investigated the impact of Zn on Pb tissue accumulation and Pb-induced toxicities. Animals (n = 6 rats per group) were exposed to lead acetate (PbAc) or a combination of PbAc and zinc acetate (ZnAc) under the following groups: control (deionized water), low PbAc [12 mg/kg PbAc (3 mg PbAc/rat/day)], low PbAc-ZnAc [12 mg/kg PbAc (3 mg PbAc/rat/day) + 0.2 mg ZnAc/rat/48 hr], high PbAc [120 mg/kg (30 mg PbAc/rat/day)], and high PbAc-ZnAc [120 mg/kg (30 mg PbAc/rat/day) + 1 mg ZnAc/rat/48 hr] for 8 weeks. A significant reduction in body weight gain was observed in the high PbAc group relative to the control group. Muscles and testes both had reduced and increased Pb uptake in low PbAc-ZnAc and high PbAc-ZnAc groups compared to PbAc only groups, respectively. Bone Pb levels in the high PbAc-ZnAc group were lower than the high PbAc group. Zinc co-administration attenuated Pb-induced inhibition of delta aminolaevulinic acid dehydratase enzyme and enhanced catalase enzyme activity at a high level of exposure. Moreover, ZnAc seems to have minimized the effects of Pb-induced mRNA dysregulation in antioxidant and antiapoptotic enzymes encoding genes. Heme oxygenase-1 was downregulated in the kidney and brain in the low PbAc group. Liver glutathione peroxidase and thioredoxin reductase-1 were downregulated in the high PbAc group. These findings suggest that zinc co-administration with lead may partially mitigate against Pb-induced toxicities.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of zinc on tissue uptake and toxicity of lead in Sprague Dawley rat

et al. 2021

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“…Flora et al [74] have examined alterations of physiological processes in lead toxicity, through oxidative mechanisms and the modulating of thiol groups as protective agents against ROS, as therapeutic intervention employing antioxidants. Ugwuja et al [75] have also demonstrated that Zn mitigates the deleterious effects of Pb including associated hematological and biochemical derangements. e report of Robitaille and Hoffer [76] has highlighted the prevalence of hypovitaminosis C or marginal Vitamin C deficiency in contemporary society and the wide-ranging clinical implications in the general population in many common clinical and social states and justification for the determination of this key antioxidant vitamin in hospitalized and ambulant patients, a situation that remains almost completely unrecognized.…”

Section: Supplements and Biotherapymentioning

confidence: 97%

In pursuit of incorporation of markers of oxidative stress in traditional biochemical panels in clinical Chemistry: A risk assessment step in diagnosis and biotherapy

Anetor

Uche

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2022

AJBPS

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Chemical pathology (clinical chemistry/biochemistry) is the branch of laboratory medicine concerned with the detection of alterations in the chemical constituents and biochemical mechanisms, which ensure health, culminating in disease. The disease itself is a pattern of response to some insult or injury resulting in a disturbed function or structure. It is often difficult to ascertain precisely the point of transition from health to a disease state. Pathological changes, including metabolic and molecular perturbations, with the potential to progress to clinical disease, are also present in healthy populations, noteworthy are the reactive oxygen species such as hydroxyl radicals with the propensity to cause oxidative DNA damage. Biochemical profiles or panels such as liver function tests, renal function tests, bone profile, lipid profile, acid-base, and critical care have served as biomarkers employed in indicating the presence of or measuring the progress of the disease, as well as the effect of treatment. Oxidative stress, an imbalance between bio-available antioxidants and reactive species, is now widely recognized as accompanying most pathological states. Hence, the exclusion of antioxidant components in biochemical profiles appears a grave oversight. Basic components of the antioxidant system, glutathione (GSH), zinc, uric acid, ascorbic acid, and α-tocopherol, may be selected for incorporation. GSH is particularly important; as a scavenger for damaging oxidative intermediates in cells, it promises to be a good predictor of disease progression and prognosis. Including the antioxidant component into traditional profiles may aid physicians in more confidently ruling out disease, enabling further investigations, and/or reassuring patients. It is proposed that redefining the traditional profiles in chemical pathology by incorporating the indexes of the antioxidant system promises considerable improvement in the risk assessment process, in disease detection and recognition of the threshold of clinical concern in disease management and biotherapy.

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