Determination of Copper and Iron in Biological Samples of Viral Hepatitis (A–E) Female Patients

Afridi, Hassan Imran; Kazi, Tasneem Gul; Kazi, Naveed; Jamali, Mohammad Khan; Sarfaraz, Raja Adil; Arain, Mohammad Balal; Kandhro, Ghulam Abbas; Shah, Abdul Qadir; Baig, Jameel Ahmed; Jalbani, Nusrat; Ansari, Rehana

doi:10.1007/s12011-008-8297-2

Cited by 12 publications

(7 citation statements)

References 36 publications

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“…This technique has a need for solubilization of the analyte and complete or partial decomposition of the matrix using convective systems, microwave ovens, or dry ashing [24,25]. The main advantage of microwave-assisted samples pretreatment is its requirement of a small amount of mineral acids and a reduction in the production of nitrous vapors [26,27].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Status of Trace and Toxic Metals in Biological Samples (Scalp Hair, Blood, and Urine) of Normal and Anemic Children of Two Age Groups

Shah

Kazi

Afridi

et al. 2010

Biol Trace Elem Res

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Anemia affects a substantial portion of the world's population, provoking severe health problems as well as important economic losses to the region in which this condition is found. This study was designed to compare the levels of essential trace and toxic elements in scalp hair, blood, and urine samples of anemic children (n = 132) with age range 1-5 and 6-10 years of both genders. For a comparative study, 134 non-anemic age- and sex-matched children as control subjects, residing in the same city, were selected. The metals in the biological samples were measured by flame atomic absorption spectrophotometry/electrothermal atomic absorption spectrometry prior to microwave-assisted acid digestion. The proposed method was validated using certified reference samples of hair, blood, and urine. The results indicated significantly lower levels of iron, copper, and zinc in the biological samples as compared to the control children of both genders (p = 0.01-0.008). The mean values of lead and cadmium were significantly high in all three biological samples of anemic children as compared to non-anemic children of both age groups (p = 0.005-0.001). The ratios of essential metal to toxic metals in the biological samples of anemic children of both age groups were significantly lower than that of controls. Deficiency of essential trace metals and high level of toxic metals may play a role in the development of anemia in the subjects under study.

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Section: Introductionmentioning

confidence: 99%

Evaluation of Status of Trace and Toxic Metals in Biological Samples (Scalp Hair, Blood, and Urine) of Normal and Anemic Children of Two Age Groups

Shah

Kazi

Afridi

et al. 2010

Biol Trace Elem Res

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“…To discriminate between these scenarios, we measured content of several metals in the urine (Figure 4). Specific excretion was expected to produce a selective increase in copper concentration, whereas a mechanism in which hepatic cell death is the primary pathway would likely change levels of several metals [12], [13]. ICP-MS analysis confirmed that Cu levels were high in Atp7b −/− urine, compared with wild-type and increased with age (Figure 4A).…”

Section: Resultsmentioning

confidence: 95%

Urinary Copper Elevation in a Mouse Model of Wilson's Disease Is a Regulated Process to Specifically Decrease the Hepatic Copper Load

et al. 2012

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Body copper homeostasis is regulated by the liver, which removes excess copper via bile. In Wilson's disease (WD), this function is disrupted due to inactivation of the copper transporter ATP7B resulting in hepatic copper overload. High urinary copper is a diagnostic feature of WD linked to liver malfunction; the mechanism behind urinary copper elevation is not fully understood. Using Positron Emission Tomography-Computed Tomography (PET-CT) imaging of live Atp7b−/− mice at different stages of disease, a longitudinal metal analysis, and characterization of copper-binding molecules, we show that urinary copper elevation is a specific regulatory process mediated by distinct molecules. PET-CT and atomic absorption spectroscopy directly demonstrate an age-dependent decrease in the capacity of Atp7b−/− livers to accumulate copper, concomitant with an increase in urinary copper. This reciprocal relationship is specific for copper, indicating that cell necrosis is not the primary cause for the initial phase of metal elevation in the urine. Instead, the urinary copper increase is associated with the down-regulation of the copper-transporter Ctr1 in the liver and appearance of a 2 kDa Small Copper Carrier, SCC, in the urine. SCC is also elevated in the urine of the liver-specific Ctr1 −/− knockouts, which have normal ATP7B function, suggesting that SCC is a normal metabolite carrying copper in the serum. In agreement with this hypothesis, partially purified SCC-Cu competes with free copper for uptake by Ctr1. Thus, hepatic down-regulation of Ctr1 allows switching to an SCC-mediated removal of copper via kidney when liver function is impaired. These results demonstrate that the body regulates copper export through more than one mechanism; better understanding of urinary copper excretion may contribute to an improved diagnosis and monitoring of WD.

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“…Previous reports have stated that the host response to HCV infection may be primarily dependent on the human leukocyte antigen system. However, other factors, such as copper, may also influence the host response because changes in copper levels in patients with HCV infection have been reported [15,36,37] . We propose that the H1069Q mutation of the ATP7B gene may be an important modifier in patients with HCV infection.…”

Section: Discussionmentioning

confidence: 99%

Association between inherited monogenic liver disorders and chronic hepatitis C

Piekuse¹,

Kreile²,

Zariņa³

et al. 2014

WJH

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AIM:To determine the frequencies of mutations that cause inherited monogenic liver disorders in patients with chronic hepatitis C. METHODS:This study included 86 patients with chronic hepatitis C (55 men, 31 women; mean age at diagnosis, 38.36 ± 14.52 years) who had undergone antiviral therapy comprising pegylated interferon and ribavirin. Viral load, biochemical parameter changes, and liver biopsy morphological data were evaluated in all patients. The control group comprised 271 unrelated individuals representing the general population of Latvia for mutation frequency calculations. The most frequent mutations that cause inherited liver disorders [gene (mutation): ATP7B (H1069Q), HFE (C282Y, H63D), UGT1A1 (TA)7, and SERPINA1 (PiZ)] were detected by polymerase chain reaction (PCR), bidirectional PCR allele-specific amplification, restriction fragment length polymorphism analysis, and sequencing. RESULTS:The viral genotype was detected in 80 of the 86 patients. Viral genotypes 1, 2, and 3 were present in 61 (76%), 7 (9%), and 12 (15%) patients, respectively. Among all 86 patients, 50 (58%) reached an early viral response and 70 (81%) reached a sustained viral response. All 16 patients who did not reach a sustained viral response had viral genotype 1. Casecontrol analysis revealed a statistically significant difference in only the H1069Q mutation between patients and controls (patients, 0.057; controls, 0.012; odds ratio, 5.514; 95%CI: 1.119-29.827, P = 0.022). However, the H1069Q mutation was not associated with antiviral treatment outcomes or biochemical indices. The (TA) 7 mutation of the UGT1A1 gene was associated with decreased ferritin levels (beta regression coefficient = -295.7, P = 0.0087). CONCLUSION:Genetic mutations that cause inherited liver diseases in patients with hepatitis C should be studied in detail.

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Determination of Copper and Iron in Biological Samples of Viral Hepatitis (A–E) Female Patients

Cited by 12 publications

References 36 publications

Evaluation of Status of Trace and Toxic Metals in Biological Samples (Scalp Hair, Blood, and Urine) of Normal and Anemic Children of Two Age Groups

Evaluation of Status of Trace and Toxic Metals in Biological Samples (Scalp Hair, Blood, and Urine) of Normal and Anemic Children of Two Age Groups

Urinary Copper Elevation in a Mouse Model of Wilson's Disease Is a Regulated Process to Specifically Decrease the Hepatic Copper Load

Association between inherited monogenic liver disorders and chronic hepatitis C

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