Dietary zinc attenuates renal lead deposition but metallothionein is not directly involved

Jamieson, Jennifer A.; Stringer, Danielle; Zahradka, Peter; Taylor, Carla G.

doi:10.1007/s10534-007-9090-y

Cited by 12 publications

(10 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…All groups except the ZD group had some staining in the lumina of renal tubules. Similar to our study, strong MT staining in renal epithelial tubular cells and in the lumen of some tubules was previously observed in rats [27][28][29]. While we did not observe MT staining in the glomerulus, others have reported upregulated MT-I mRNA levels at this site in response to oxidative stress [30].…”

Section: Article In Presssupporting

confidence: 91%

“…Similar effects of zinc deficiency on renal zinc and/or MT were observed in the kidney of rat pups, weanling rats and adult rats [23][24][25][26][27][28], paralleled by lower MT-1 and MT-2 mRNA in renal tissue [13,26]. Collectively, these results confirm that renal MT is synthesized in response to dietary zinc, as further evidenced by the correlation between kidney zinc and MT concentrations (Fig.…”

Section: Discussionsupporting

confidence: 78%

See 1 more Smart Citation

Renal metallothionein responds rapidly and site specifically to zinc repletion in growing rats

Szczurek

Bjornsson

Noto

et al. 2009

Journal of Trace Elements in Medicine and Biology

Self Cite

View full text Add to dashboard Cite

Section: Article In Presssupporting

confidence: 91%

Section: Discussionsupporting

confidence: 78%

Renal metallothionein responds rapidly and site specifically to zinc repletion in growing rats

Szczurek

Bjornsson

Noto

et al. 2009

Journal of Trace Elements in Medicine and Biology

Self Cite

View full text Add to dashboard Cite

“…Zn supplementation reduces heavy metal (such as lead and cadmium) absorption and tissue accumulation and, as a result, reduces heavy metal cytotoxicity . Here, we report that pre‐treating cells with Zn (100 μM) for 24 hr prior to exposure to 500 μM DU for 24 hr can significantly increase cell viability.…”

Section: Discussionsupporting

confidence: 92%

Zinc Protects Human Kidney Cells from Depleted Uranium‐induced Apoptosis

Hao

Ren

Liu

et al. 2013

Basic Clin Pharma Tox

View full text Add to dashboard Cite

Depleted uranium (DU) is a weak radioactive heavy metal, and zinc (Zn) is an effective antidote to heavy metal poisoning. However, the effect of Zn on DU-induced cytotoxicity and apoptosis is not completely understood. The purpose of this study was to evaluate the effect of Zn on DU-induced cell apoptosis in human kidney cells (HK-2) and explore its molecular mechanism. Pre-treatment with Zn significantly inhibited DU-induced apoptosis. It reduced the formation of reactive oxygen species in the cells, increased the catalase (CAT) and glutathione (GSH) concentrations, suppressed the DU-induced soluble Fas receptor (sFasR) and soluble Fas ligand (sFasL) overexpression, suppressed the release of cytochrome c and apoptosis inhibitor factor (AIF) from mitochondria to cytoplasm, inhibited the activation of caspase-9, caspase-8 and caspase-3, and induced metallothionein (MT) expression. Furthermore, exogenous MT effectively inhibited DU-induced cell apoptosis. In conclusion, mitochondrial and FasR-mediated apoptosis pathways contribute to DU-induced apoptosis in HK-2 cells. Through independent mechanisms, such as indirect antioxidant effects, inhibition of the activation of caspase-9, caspase-8 and caspase-3, and induction of MT expression, Zn inhibits DU-induced apoptosis.Due to its high density and affordability, depleted uranium (DU) has been widely used in civilian and military activities. However, unregulated release of DU into the environment during its production and use could cause DU to enter the human body through the respiratory tract, gastrointestinal tract or skin, after which DU is distributed to bones, kidney, liver or reproductive organs, becoming a threat to human health [1].Depleted uranium has the dual effects of radioactive and heavy metal toxicities, particularly heavy metal toxicity [2,3]. The chemical toxicity of acute, high DU exposure especially targets the kidneys, causing severe renal proximal tubular necrosis, renal failure and, ultimately, death [4]. Kidney damage is caused when the uranium intake exceeds 2 mg/kg body-weight [5] or when kidney uranium deposition reaches 3 lg/g in a short time [6]. When human beings are exposed to high doses of DU in a short period of time, a decrease in glomerular filtration rate and increase in serum creatinine, urine protein and urine catalase (CAT) are observed [7,8]. Shim et al. [9] reported that on day 6 after one dose of uranyl nitrate intraperitoneal injection (0.5 mg/kg) in Sprague-Dawley rats, serum creatinine and blood urea nitrogen (BUN) were increased, and the creatinine clearance rate was decreased. Our preliminary study [4] demonstrated that one dose of uranyl acetate in rats via intraperitoneal injection (10 mg/kg, 4 days after injection) increased the uranium level in urine, liver, spleen and kidney. Moreover, higher serum creatinine, BUN and urinary N-acetyl-b-D glucosaminidase (NAG) were detected. A large number of casts, hyaline degeneration and vacuolization, and even shedding and necrosis of renal tubular epithelial cells, wer...

show abstract

“…The animals were randomly assigned into five groups (ten animals each) and fed one of the following diets and drinking water: American Institute of Nutrition (AIN)-76 diet (control diet) and tap water (control group, Control), AIN-76 diet and 200 mg/l lead acetate water (Pb-exposed group, Pb), and AIN-76 modified diet plus 2, 5 or 10% CV (CV diet) and 200 mg/l lead acetate water (Pb+CV2, Pb+CV5, Pb+CV10). The dose level of Pb was designed as described by Jamieson et al 43) with modification. This concentration was chosen to produce a sub-clinical toxicity, as the dosage given for 10 weeks with a standard laboratory rat chow has shown not to produce significant alterations in hematopoiesis, histology and function.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Chlorella vulgaris against Lead-Induced Oxidative Stress in Rat Brains

Yun

Kim

Kwon

et al. 2011

JOURNAL OF HEALTH SCIENCE

View full text Add to dashboard Cite

Lead (Pb) is a toxic heavy metal widely distributed in the environment. Recent studies suggest oxidative stress as one possible mechanism involved in Pb poisoning. The unicellular algae Chlorella vulgaris (CV) contains various bioactive substances with antioxidant for the prevention of oxidative stress by metals. We investigated the protective effects of CV on the oxidative system in five groups of male Sprague-Dawley rats fed American Institute of Nutrition (AIN)-76 diet, plus 2, 5 or 10% CV for 4 weeks. All animals were exposed to 200 mg/l lead acetate by drinking water except for the control (tap water). Body weight gains were significantly reduced in the Pb-exposed group (64%) relative to the control and CV groups. Brain weights were significantly increased in the Pb-exposed group (44%) relative to the others. In the experimental period, food intake, water intake and Pb intake were not different among the groups. The levels of Pb (87%) in brain obtained from the Pb-exposed group were significantly increased compared to the other groups. The levels of oxidative stress parameters in the brain such as superoxide dismutase (36%), glutathione peroxidase (63%), and glutathione reductase (30%) were decreased in the Pb-exposed group relative to the control but markedly increased in the CV groups. The CV also significantly increased glutathione levels by approximately 1.7-fold over the Pb-exposed group, while the malondialdehye concentration significantly decreased by approximately 47-71%. Based on these results, we found alterations in several indicators of oxidative stress of Pb intoxication, suggesting the antioxidant potential of CV. Therefore, CV may have protective effects on brain damage of low-level and short-term Pb exposure in the brains of rats.

show abstract

Dietary zinc attenuates renal lead deposition but metallothionein is not directly involved

Cited by 12 publications

References 33 publications

Renal metallothionein responds rapidly and site specifically to zinc repletion in growing rats

Renal metallothionein responds rapidly and site specifically to zinc repletion in growing rats

Zinc Protects Human Kidney Cells from Depleted Uranium‐induced Apoptosis

Protective Effect of Chlorella vulgaris against Lead-Induced Oxidative Stress in Rat Brains

Contact Info

Product

Resources

About