Growth performance and oxidative damage in kidney induced by oral administration of Cr(III) in chicken

Liu, Yanhan; Liu, Cun; Cheng, Jia; Fan, Wentao; Zhang, Xiao; Liu, Jianzhu

doi:10.1016/j.chemosphere.2015.07.032

Cited by 15 publications

(5 citation statements)

References 37 publications

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“…The SOD activity was determined using the nitro blue tetrazolium method [ 28 ]. This protocol is based on the ability of the enzyme to inhibit the phenazine-methosulfate-mediated reduction of nitro blue tetrazolium dye.…”

Section: Methodsmentioning

confidence: 99%

Vitamin E Supplementation Ameliorates Newcastle Disease Virus-Induced Oxidative Stress and Alleviates Tissue Damage in the Brains of Chickens

Rehman

Qiu

Sun

et al. 2018

Viruses

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Newcastle disease (ND), characterized by visceral, respiratory, and neurological pathologies, causes heavy economic loss in the poultry industry around the globe. While significant advances have been made in effective diagnosis and vaccine development, molecular mechanisms of ND virus (NDV)-induced neuropathologies remain elusive. In this study, we report the magnitude of oxidative stress and histopathological changes induced by the virulent NDV (ZJ1 strain) and assess the impact of vitamin E in alleviating these pathologies. Comparative profiling of plasma and brains from mock and NDV-infected chicken demonstrated alterations in several oxidative stress makers such as nitric oxide, glutathione, malondialdehyde, total antioxidant capacity, glutathione S-transferase, superoxide dismutase, and catalases. While decreased levels of glutathione and total antioxidant capacity and increased concentrations of malondialdehyde and nitric oxide were observed in NDV-challenged birds at all time points, these alterations were eminent at latter time points (5 days post infection). Additionally, significant decreases in the activities of glutathione S-transferase, superoxide dismutase, and catalase were observed in the plasma and brains collected from NDV-infected chickens. Intriguingly, we observed that supplementation of vitamin E can significantly reduce the alteration of oxidative stress parameters. Under NDV infection, extensive histopathological alterations were observed in chicken brain including neural inflammation, capillary hyperemia, necrosis, and loss of prominent axons, which were reduced with the treatment of vitamin E. Taken together, our findings highlight that neurotropic NDV induces extensive tissue damage in the brain and alters plasma oxidative stress profiles. These findings also demonstrate that supplementing vitamin E ameliorates these pathologies in chickens and proposes its supplementation for NDV-induced stresses.

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Section: Methodsmentioning

confidence: 99%

Vitamin E Supplementation Ameliorates Newcastle Disease Virus-Induced Oxidative Stress and Alleviates Tissue Damage in the Brains of Chickens

Rehman

Qiu

Sun

et al. 2018

Viruses

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“…Cr accumulates in large quantities in the heart, liver, and kidneys over a long period of time and leads to impaired metal absorption and metabolism in chickens (Liu et al, 2016). Oral administration of CrCl 3 can reduce the growth performance of chickens, cause pathological lesions such as renal tubular atrophy and structural degeneration of the glomerulus, and affect the antioxidant capacity of the kidney (Liu et al, 2015). The addition of different concentrations of CrCl 3 to drinking water induces oxidative stress in the chicken brain, and Cr(III) at doses up to 50.00% can significantly increase the levels of malondialdehyde and hydrogen peroxide in brain tissue (Cheng et al, 2016).…”

Section: Accumulative Poisoningmentioning

confidence: 99%

Toxicity mechanisms and remediation strategies for chromium exposure in the environment

Yan

Ying-jun

Xue

et al. 2023

Front. Environ. Sci.

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Chromium (Cr) is the seventh most abundant chemical element in the Earth’s crust, and Cr(III) and Cr(VI) are common stable valence states of Cr. Several Cr-containing substances, such as FeOCr2O3 and stainless-steel products, exist in nature and in life. However, Cr(VI) is toxic to soil, microorganisms, and plants and poses a serious threat to human health through direct and indirect exposure. By collecting published journal literature, we found that Cr(VI) can cause acute and chronic toxicity in organisms and has carcinogenic effects, and the mechanisms causing these toxicity include endoplasmic reticulum stress, autophagy and apoptosis. However, the relationship between these mechanisms remains unclear. Many methods have been researched to purify chromium, but each of these methods has its own advantages and disadvantages. Therefore, this review summarizes the hazards of chromium and the mechanisms of chromium toxicity after entering cells and provides a number of methods for chromium contamination management, providing a direction for the next step in chromium toxicology and contamination decontamination research.

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“…For example, Cr(III) is regarded as an essential micronutrient that is often found in many dietary supplements to promote cellular homeostasis. 3−5 This is due to its involvement with low-molecular-weight chromium-binding-substance that maintains the active conformation of the insulin receptor, important for blood glucose regulation. However, high concentrations of Cr(III) exposure can lead to toxicity.…”

Section: Introductionmentioning

confidence: 99%

“…The toxicity of metals in the body can also be dependent on the metal oxidation state. For example, Cr(III) is regarded as an essential micronutrient that is often found in many dietary supplements to promote cellular homeostasis. − This is due to its involvement with low-molecular-weight chromium-binding-substance that maintains the active conformation of the insulin receptor, important for blood glucose regulation. However, high concentrations of Cr(III) exposure can lead to toxicity. − On the other hand, Cr(VI) is known to induce oxidative stress, cytotoxicity, and carcinogenicity, regardless of its concentration. ,,− …”

Section: Introductionmentioning

confidence: 99%

“…Elevated levels of Cr(III) have been associated with heightened production of reactive oxygen species (ROS). ,,,− In some cases, Cr(III) has been shown to lead to higher ROS levels than the toxic Cr(VI) oxidation state . The mechanism of Cr(III) toxicity is believed to involve not only elevated levels of ROS, but also the direct interaction of Cr(III) with DNA.…”

Section: Introductionmentioning

confidence: 99%

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Correlating Live Cell Viability with Membrane Permeability Disruption Induced by Trivalent Chromium

Filice

Henderson

et al. 2019

ACS Omega

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Cr(III) is often regarded as a trace essential micronutrient that can be found in many dietary supplements due to its participation in blood glucose regulation. However, increased levels of exposure have been linked to adverse health effects in living organisms. Herein, scanning electrochemical microscopy (SECM) was used to detect variation in membrane permeability of single cells (T24) resulting from exposure to a trivalent Cr-salt, CrCl3. By employing electrochemical mediators, ferrocenemethanol (FcMeOH) and ferrocenecarboxylic acid (FcCOO–), initially semipermeable and impermeable, respectively, complementary information was obtained. Three-dimensional COMSOL finite element analysis simulations were successfully used to quantify the permeability coefficients of each mediator by matching experimental and simulated results. Depending on the concentration of Cr(III) administered, three regions of membrane response were detected. Following exposure to low concentrations (up to 500 μM Cr(III)), their permeability coefficients were comparable to that of control cells, 80 μm/s for FcMeOH and 0 μm/s for FcCOO–. This was confirmed for both mediators. As the incubation concentrations were increased, the ability of FcMeOH to permeate the membrane decreased to a minimum of 17 μm/s at 7500 μM Cr(III), while FcCOO– remained impermeable. At the highest examined concentrations, both mediators were found to demonstrate increased membrane permeability. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell viability studies were also conducted on Cr(III)-treated T24 cells to correlate the SECM findings with the toxicity effects of the metal. The viability experiments revealed a similar concentration-dependent trend to the SECM cell membrane permeability study.

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Growth performance and oxidative damage in kidney induced by oral administration of Cr(III) in chicken

Cited by 15 publications

References 37 publications

Vitamin E Supplementation Ameliorates Newcastle Disease Virus-Induced Oxidative Stress and Alleviates Tissue Damage in the Brains of Chickens

Vitamin E Supplementation Ameliorates Newcastle Disease Virus-Induced Oxidative Stress and Alleviates Tissue Damage in the Brains of Chickens

Toxicity mechanisms and remediation strategies for chromium exposure in the environment

Correlating Live Cell Viability with Membrane Permeability Disruption Induced by Trivalent Chromium

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