Arsenic Toxicology:  Five Questions

Aposhian, H. Vasken; Aposhian, Mary M.

doi:10.1021/tx050106d

Cited by 258 publications

(152 citation statements)

References 88 publications

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“…2004; Emadi and Gore 2010). Unsurprisingly, investigations in noncancerous cells and in rodents suggested that some of these side effects could be secondary to oxidative stress and mitochondrial dysfunction (Aposhian and Aposhian 2006; Jomova et al. 2011; Mathews et al.…”

Section: Introductionmentioning

confidence: 99%

Role of endoplasmic reticulum stress in drug‐induced toxicity

Foufelle

Fromenty

2016

Pharmacology Res & Perspec

181

161

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Drug‐induced toxicity is a key issue for public health because some side effects can be severe and life‐threatening. These adverse effects can also be a major concern for the pharmaceutical companies since significant toxicity can lead to the interruption of clinical trials, or the withdrawal of the incriminated drugs from the market. Recent studies suggested that endoplasmic reticulum (ER) stress could be an important event involved in drug liability, in addition to other key mechanisms such as mitochondrial dysfunction and oxidative stress. Indeed, drug‐induced ER stress could lead to several deleterious effects within cells and tissues including accumulation of lipids, cell death, cytolysis, and inflammation. After recalling important information regarding drug‐induced adverse reactions and ER stress in diverse pathophysiological situations, this review summarizes the main data pertaining to drug‐induced ER stress and its potential involvement in different adverse effects. Drugs presented in this review are for instance acetaminophen (APAP), arsenic trioxide and other anticancer drugs, diclofenac, and different antiretroviral compounds. We also included data on tunicamycin (an antibiotic not used in human medicine because of its toxicity) and thapsigargin (a toxic compound of the Mediterranean plant Thapsia garganica) since both molecules are commonly used as prototypical toxins to induce ER stress in cellular and animal models.

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Section: Introductionmentioning

confidence: 99%

Role of endoplasmic reticulum stress in drug‐induced toxicity

Foufelle

Fromenty

2016

Pharmacology Res & Perspec

181

161

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“…Organic species derived primarily from seafood such as arsenobetaine (AsB) or arsenosugars can be identified, as can the contribution of toxic species. The metabolism of inorganic arsenic in humans results in methylarsonate (MMA) and dimethylarsinate (DMA), which are excreted together in urine (Aposhian and Aposhian, 2006). Organoarsenicals are also excreted in urine, but they have low or no toxicity compared with inorganic arsenic (Francesconi and Kuehnelt, 2004).…”

Section: Introductionmentioning

confidence: 99%

Urinary arsenic species, toenail arsenic, and arsenic intake estimates in a Michigan population with low levels of arsenic in drinking water

Rivera‐Núñez

Meliker

Meeker

et al. 2011

J Expo Sci Environ Epidemiol

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The large disparity between arsenic concentrations in drinking water and urine remains unexplained. This study aims to evaluate predictors of urinary arsenic in a population exposed to low concentrations (r50 mg/l) of arsenic in drinking water. Urine and drinking water samples were collected from a subsample (n ¼ 343) of a population enrolled in a bladder cancer case-control study in southeastern Michigan. Total arsenic in water and arsenic species in urine were determined using ICP-MS: arsenobetaine (AsB), arsenite ( A separate analysis indicated that AsB and DMA [V] were significantly correlated with fish and shellfish consumption, which may suggest that seafood intake influences DMA[V] excretion. The Spearman correlation between arsenic concentration in toenails and SumAs was 0.36 and between arsenic concentration in toenails and arsenic concentration in water was 0.42. Results show that arsenic exposure from drinking water consumption is an important determinant of urinary arsenic concentrations, even in a population exposed to relatively low levels of arsenic in drinking water, and suggest that seafood intake may influence urinary DMA [V] concentrations.

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“…Moreover, oxidative stress also causes cell death in arsenic intoxicated animals. Pyruvate dehydrogenase enzyme, used in the citric acid cycle, is inhibited by arsenic metabolites; as a result of disturbed cell energy production (Aposhian & Aposhian 2006), hosts would experience lack of weight gain.…”

Section: Discussionmentioning

confidence: 99%

Immunosuppressive effects of arsenic in broiler chicks exposed to Newcastle disease virus

Sattar

Khan

Hussain

et al. 2016

Journal of Immunotoxicology

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To assess the effects of prolonged exposure to arsenic (As, as arsenate) on host immune competence overall and resistance to Newcastle disease (ND) viral infection in particular, a study was carried out in broiler chicks. At 7 days of age, chicks were assigned to groups that would undergo varying vaccination, challenge, and/or As exposures; Group 1 was a control; Group 2 was to receive Newcastle disease virus (NDV) only; two groups (Groups 3, 4) were to be given As daily (50 mg/kg, by gavage) from Days 7-35 of the experiment. All groups underwent normal vaccination on Days 5, 23, and 32 against live NDV (B1 type, LaSota strain); two groups (Groups 2, 4) were challenged with field-isolated NDV at Day 24. At Days 14, 21, 28, and 35 of age, subsets of chicks in each group were evaluated. The results showed feed intake and weight gain were lower in As-treated and NDV-challenged chicks. In As-treated chicks, absolute and relative spleen weights were significantly greater, whereas those of the thymus significantly lower, over the entire 35-day period. Effects on bursa weights (absolute, relative) were only significantly reduced through Day 21. Antibody titers against ND were significantly reduced (vs. control) over the whole 35 days in birds that received As alone, but only significantly depressed through the first 21 days in birds that received As þ NDV; thereafter, titers were significantly greater (in parallel with effects in birds that received NDV alone). In contrast, antibody responses to T-dependent antigen (Sheep red blood cells [SRBC]) were significantly lower in As only-and As þ NDV-treated chicks throughout the study period. Among birds exposed to As (alone or with NDV), in situ phagocytic activity was elevated and cutaneous sensitivity responses decreased during the period from Day 28 to Day 35. NDV alone had spurious effects on phagocytic activity but did cause significant reductions in cutaneous sensitivity responses. It was concluded that arsenic decreased immunity in broiler chicks, thereby making them prone to ND. ARTICLE HISTORY

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Arsenic Toxicology: Five Questions

Cited by 258 publications

References 88 publications

Role of endoplasmic reticulum stress in drug‐induced toxicity

Role of endoplasmic reticulum stress in drug‐induced toxicity

Urinary arsenic species, toenail arsenic, and arsenic intake estimates in a Michigan population with low levels of arsenic in drinking water

Immunosuppressive effects of arsenic in broiler chicks exposed to Newcastle disease virus

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