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- Bergdahl, Ingvar A., et al.
(författare)
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Non-renal effects and the risk assessment of environmental cadmium exposure.
- 2014
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Ingår i: Environmental health perspectives. - : Environmental Health Perspectives. - 1552-9924 .- 0091-6765. ; 122:5, s. 431-8
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Tidskriftsartikel (refereegranskat)abstract
- Exposure to cadmium (Cd) has long been recognized as a health hazard, both in industry and in general populations with high exposure. Under the currently prevailing health risk assessment, the relationship between urinary Cd (U-Cd) concentrations and tubular proteinuria is used. However, doubts have recently been raised regarding the justification of basing the risk assessment on this relationship at very low exposure.
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| 5. |
- Broberg, Karin, et al.
(författare)
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Gene-Environment Interactions for Metals
- 2014. - 4th
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Ingår i: Handbook on the Toxicology of Metals. - 9780444594532 - 9780123973399 ; 1, s. 239-264
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Bokkapitel (refereegranskat)abstract
- It has become increasingly clear that the individual genetic background influences susceptibility to metal toxicity. Genetic variation in genes that regulate metal toxicokinetics and toxicodynamics influence the degree of metal accumulation and retention in the body, as well as toxic effects. Moreover, factors that regulate gene expression, so-called epigenetic factors, have been identified as targets for metal toxicity. This chapter addresses what is currently known about such gene-environment interactions. The picture that emerges for most metals is that the genetic influence is probably not attributed to a single gene for each metal; rather it is polygenic, with some genes having a stronger effect than others. The presence of variants of the human leukocyte antigen system and the risk of beryllium-related pulmonary disease was one of the first and maybe the strongest example of a gene-environment interaction. There are also clear gene-environment interactions for arsenic and lead. Evidence is rapidly growing for epigenetic effects of metals, e.g. for arsenic, cadmium, and lead, which may explain the association between metal exposure early in life and toxic effects later in life, as well as metal carcinogenicity.
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- Liang, Yihuai, et al.
(författare)
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Increased hepatic and decreased urinary metallothionein in rats after cessation of oral cadmium exposure
- 2010
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Ingår i: Basic & Clinical Pharmacology & Toxicology. - : John Wiley & Sons. - 1742-7835 .- 1742-7843. ; 106:4, s. 348-355
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Tidskriftsartikel (refereegranskat)abstract
- We investigated the role of metallothionein (MT) in tissues after cessation of cadmium (Cd) exposure. Wistar rats of both genders were given CdCl(2) in drinking water at daily doses of 0, 2.5, 5.0 or 10.0 mg Cd/kg body-weight for 12 weeks. Half of the animals were then killed; the others were given Cd-free water for the following 16 weeks, i.e. until 28 weeks after start of the experiment (28-week rats). We observed dose-dependent increases in the levels of MT in the tissues of rats 12 weeks after beginning the experiment (12-week rats). After the exposure ceased, levels of MT in the 28-week rats changed in three ways: an increase in the liver, persistence in the kidney cortex and a decrease in the medulla, relative to those levels in their 12-week counterparts. Biomarkers of kidney dysfunction were determined to be urinary MT (UMT) and urinary N-acetyl-beta-d-glucosaminidase (UNAG). After 12 weeks, we observed dose-related statistically significant increases in UMT and UNAG in all of the Cd-exposed groups. A statistically significant decrease for UNAG between the 12- and 28-week rats occurred among males at the lowest Cd dose and for UMT in all of the Cd-exposed groups. The unchanged tissue levels of MT in the kidney cortex suggest that decreased UMT is a sign either of (i) decreased transport of Cd-MT from the liver via blood plasma to the renal tubules or (ii) increased tubular reabsorption and recovery of renal tubular function.
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| 7. |
- Liang, Yihuai, et al.
(författare)
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Renal function after reduction in cadmium exposure : an eight-year follow-up of residents in cadmium-polluted areas
- 2012
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Ingår i: Journal of Environmental Health Perspectives. - : National Institute of Environmental Health Sciences. - 0091-6765 .- 1552-9924. ; 120:2, s. 223-228
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Tidskriftsartikel (refereegranskat)abstract
- Background and objective: Long-term exposure to cadmium (Cd) causes renal dysfunction, but its change with exposure is unknown. We aimed at assessing the evolution of Cd-induced renal effects after a reduction in dietary exposure to Cd in rice.Methods: 412 residents in previously Cd-polluted and non-polluted areas were examined twice: in 1998 and 2006. Changes in blood Cd, urinary Cd, and kidney function (N-acetyl-β-D-glucosaminidase = NAG, β2-microglobulin, and albumin in urine) were measured. Results: In the most polluted area, mean blood Cd was 8.9 μg/L in 1998 and 3.3 μg/L in 2006, and urinary Cd was 11.6 and 9.0 μg/g creatinine in 1998 and 2006, respectively. Urinary albumin in 1998 increased with urinary Cd but no such exposure-response appeared for 2006 albumin versus urinary Cd 1998, indicating recovery. Other biomarkers of kidney function were also elevated in 1998. Partial recovery was observed for NAG, among women, and suggested for β2-microglobulin, among young individuals. The probability of having a β2-microglobulin above the 95th percentile in 2006 was high in those with an elevated β2-microglobulin in 1998 (odds ratio: 24.8, 95% CI: 11.2-55.3), whereas corresponding estimates for albumin and NAG were 3.0 (1.2-7.5) and 2.6 (1.6-4.4), respectively.Conclusions: Results suggest that a Cd-mediated increase in urinary albumin excretion is reversible upon substantial reduction of exposure. For the markers of tubular effects, a tendency towards improvement, but not complete recovery, was observed. Data from repeated observations suggests that β2-microglobulin may be more informative than NAG as an indicator for the individual's future tubular function.
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| 8. |
- Nordberg, Gunnar, et al.
(författare)
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Kidney dysfunction and cadmium exposure : Factors influencing dose-response relationships
- 2012
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Ingår i: Journal of Trace Elements in Medicine and Biology. - : Elsevier BV. - 0946-672X .- 1878-3252. ; 26:2-3, s. 197-200
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Tidskriftsartikel (refereegranskat)abstract
- Our early toxicological studies showed that metallothionein (MT) is a protein that carries cadmium (Cd) to the kidney, explaining why Cd exposures during long time periods may give rise to kidney dysfunction. This dysfunction is usually considered to be the critical effect, i.e. the adverse effect that occurs at the lowest exposure level. MT also provides intracellular protection against cadmium toxicity. In studies of population groups in cadmium contaminated areas in China, we investigated factors that affected the relationship between internal dose of Cd, as indicated by blood Cd (BCd) or urinary Cd (UCd), and the prevalence of kidney dysfunction. We found dose-response relationships between UCd and the prevalence of increased levels of biomarkers of renal tubular dysfunction (urinary beta-2-microglobulin, B2M, or N-acetyl-beta-D-glucosaminidase - NAG) or urinary albumin (UAlb), a biomarker of glomerular kidney dysfunction. Two years after Cd intake from contaminated rice was diminished, renal tubular dysfunction appeared unchanged or aggravated among those with higher UCd; Another 8 years later, i.e. 10 years after Cd intake was decreased, the prevalence of renal tubular dysfunction was still increased but UAlb had returned to normal. Factors that influenced the dose-response relationships were: (1) time after maximum exposure. (2) Concomitant exposure to other nephrotoxic agents such as inorganic arsenic. (3) Cd induced metallothionein mRNA levels in peripheral blood lymphocytes, used as a biomarker of the ability of each person, to synthesize MT. (4) The occurrence of increased levels in blood plasma of autoantibodies against MT. The two last points further support a role in humans of MT as a protective protein against tissue damage from cadmium and gives support to previous ideas developed partly in experimental systems.
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| 9. |
- Ekman, Anna, et al.
(författare)
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Bioresource utilisation by sustainable technologies in new value-added biorefinery concepts - two case studies from food and forest industry
- 2013
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Ingår i: Journal of Cleaner Production. - : Elsevier BV. - 0959-6526 .- 1879-1786. ; 57, s. 46-58
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Tidskriftsartikel (refereegranskat)abstract
- This paper presents a trans-disciplinary assessment of new and innovative biorefinery concepts producing high-value chemical compounds from residues from agriculture, food and forest industries. There is a significant potential of biomass residues in Sweden suitable for the extraction of various compounds, including upgrading by biocatalytic processes, in addition to current energy generation. Two examples presented are quercetin extracted from onion waste by pressurised hot water in conjunction with enzymatic hydrolysis, and betulin from birch bark extracted by liquid CO2 containing ethanol. Inherent in these two extraction processes and production routes is the ability to show good environmental performance from a life cycle perspective. Extraction of high-value compounds also provides possibilities for innovation in the current agricultural, food and forest industry potentially leading to socio-economical benefits. (C) 2013 The Authors. Published by Elsevier Ltd. All rights reserved.
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| 10. |
- Roos, Per M., et al.
(författare)
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Manganese in cerebrospinal fluid and blood plasma of patients with amyotrophic lateral sclerosis
- 2012
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Ingår i: Experimental biology and medicine. - : SAGE Publications. - 1535-3702 .- 1535-3699. ; 237:7, s. 803-810
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Tidskriftsartikel (refereegranskat)abstract
- Neurotoxic properties of manganese (Mn) are well documented. It is less known that Mn contributes to the development of neurodegenerative disorders in the general population. This study presents Mn data from patients with amyotrophic lateral sclerosis (ALS) in a well-defined cohort diagnosed by electrophysiological methods. Cerebrospinal fluid (CSF) and plasma were collected from patients and controls. Mn concentrations were analyzed by high-resolution inductively coupled plasma mass spectrometry. Concentrations of Mn were significantly higher in ALS CSF (median 5.67 mu g/L) than in CSF from controls (median 2.08 mu g/L). Also, ALS CSF Mn concentrations were higher than ALS plasma Mn concentrations (median 0.91 mu g/L), suggesting transport of Mn into the central nervous system. The properties of barrier systems between blood and the brain are discussed and the possibility of Mn accumulation contributing to the relentless course of ALS is introduced.
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