Antagonistic effect of N-acetyl-L-cysteine against cadmium-induced cytotoxicity and abnormal immune response on chicken peritoneal macrophages

Zhang, Ding; Yang, Xiaoyu; Qin, Ying-ze; Wu, Guodong; Ning, Guan-bao; Huo, Nairui; Tian, Wen‐xia

doi:10.1016/j.ecoenv.2020.111185

Cited by 19 publications

(10 citation statements)

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“…A recent study showed that LPS activates immunity-related processes in macrophages, whereas Cd inhibits these processes (62). An in-vivo study by Zhang et al showed that Cd (20 mM and 50 mM) dose-dependently caused morphological and ultrastructural damage in chicken peritoneal macrophages, ROS accumulation, and mitochondrial injury (46). Furthermore, Cd exposure inhibited the activity of chicken peritoneal macrophages and promoted the expression of IL-1b, IL-6, and TNF-a in both inactivated macrophages and cells in response to LPS stimuli (46).…”

Section: And M1 Macrophagesmentioning

confidence: 99%

“…An in-vivo study by Zhang et al showed that Cd (20 mM and 50 mM) dose-dependently caused morphological and ultrastructural damage in chicken peritoneal macrophages, ROS accumulation, and mitochondrial injury (46). Furthermore, Cd exposure inhibited the activity of chicken peritoneal macrophages and promoted the expression of IL-1b, IL-6, and TNF-a in both inactivated macrophages and cells in response to LPS stimuli (46). Similarly, in mammals, long-term Cd exposure can result in reduced expression of cytokines, such as IL-1 and TNF-a, and inhibition of macrophage activity (72).…”

Section: And M1 Macrophagesmentioning

confidence: 99%

“…Macrophages Cd promotes macrophage TNF-a, IL-6, IL-1, NO, and catalase activity Glycine reduces Cd-induced alterations in the viability and activation of macrophages (84) Cd accumulated in macrophages and produces toxicity Metallothionein intervention can be combined with Cd to inhibit Cd-induced toxicity (85) Cd inhibits the phagocytotic activity of chicken peritoneal macrophages Antagonistic effect of N-acetyl-L-cysteine against Cd-induced Cytotoxicity (46) Cd caused dose-dependent morphologic and ultrastructural alterations in macrophages Zn against Cd cytotoxicity in macrophages (112) Neutrophiles Cd caused apoptosis by endoplasmic reticulum stress Se can be antagonists with cd, effectively protecting chicken neutrophils from changes caused by Cd. Cd has cytotoxicity and genotoxicity to human lymphocytes Catechin hydrate can inhibit the anti-genotoxicity and anti-cytotoxicity of Cd by inhibiting the expression of related apoptotic genes (130)…”

Section: And Cells Toxic Effects On Cells Detoxification Mechanism Referencementioning

confidence: 99%

“…Micromolar concentrations of Cd activate multiple signaling pathways, in particular, the nuclear factor kappa B (NF-kB) and mitogen-activated protein kinase (MAPK) pathways, in immune cells and induce the upregulation of inflammatory markers and mediators (36,38,40). In addition, Cd can induce ROS production, cause mitochondrial injury, reduce antioxidant enzyme activity, induce the oxidative stress response, and activate endoplasmic reticulum stress (ERS) pathways, thereby playing a proinflammatory role in immune cells (41)(42)(43)(44)(45)(46)(47)(48). Thus, Cd affects various cell functions, including the regulation of immune-cell activity and the secretion of cytokines in innate and adaptive immunity.…”

Section: Introductionmentioning

confidence: 99%

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Effects of Cadmium Exposure on the Immune System and Immunoregulation

et al. 2021

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Cadmium (Cd), a biologically non-essential heavy metal, is widespread in the environment, including the air, water, and soil, and is widely present in foods and quantum dot preparations. Cd enters the body primarily through inhalation and ingestion. Its biological half-life in humans is 10–35 years; therefore, Cd poses long-term health risks. While most studies on Cd toxicity have focused on organ and tissue damage, the immunotoxicity of Cd has drawn increasing attention recently. Cd accumulates in immune cells, modulates the function of the immune system, triggers immunological responses, and leads to diverse health problems. Cd acts as an immunotoxic agent by regulating the activity and apoptosis of immune cells, altering the secretion of immune cytokines, inducing reactive oxygen species (ROS) production and oxidative stress, changing the frequency of T lymphocyte subsets, and altering the production of selective antibodies in immune cells. This review summarizes the immunological toxicity of Cd, elucidates the mechanisms underlying Cd toxicity in terms of innate immunity and adaptive immunity, and discusses potential strategies to alleviate the adverse effects of Cd on the immune system.

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Section: And M1 Macrophagesmentioning

confidence: 99%

Section: And M1 Macrophagesmentioning

confidence: 99%

Section: And Cells Toxic Effects On Cells Detoxification Mechanism Referencementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of Cadmium Exposure on the Immune System and Immunoregulation

et al. 2021

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“…Feed is one of the main sources of cadmium in livestock, and cereal is the most significant contributor to the dietary intake of Cd (3). It has been confirmed that Cd can cause kidney and liver damage in poultry (4)(5)(6)(7). Recently, Shen et al (8) found that the deposition of Cd in cartilage had been overlooked in the past (8).…”

Section: Introductionmentioning

confidence: 99%

Cadmium Toxicity on Chondrocytes and the Palliative Effects of 1α, 25-Dihydroxy Vitamin D3 in White Leghorns Chicken's Embryo

Wang

et al. 2021

Front. Vet. Sci.

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Cadmium (Cd) can causes osteoporosis and joint swelling. However, the mechanism of Cd toxicity in chondrocytes and how to alleviate Cd poisoning to chondrocytes are still unclear. Herein, we evaluated the toxicity of Cd to chicken chondrocytes, and whether vitamin D can relieve the toxicity of Cd to chondrocytes. Primary chondrocytes were collected from knee-joint cartilage of 15-day-old chicken embryos. They were treated with (0, 1, 2, and 4) μM Cd alone, 10−8 M 1α,25-(OH)2D3 alone, or 2 μM Cd combined with 10−8 M 1α,25-(OH)2D3. We found that Cd significantly inhibited Sox9 and ACAN mRNA expression, which are markers for chondrocyte differentiation, downregulated the mitochondrial membrane potential, upregulated the Bax/B-cell lymphoma 2 ratio. Furthermore, Cd significantly promoted matrix metalloproteinase (MMP)-9 expression, thus accelerating the degradation of extracellular matrix. And Cd also inhibited the expression of main macromolecular protein of extracellular matrix, Collagen type IIα1 (COL2A1) and acid mucopolysaccharide. However, 1α,25-(OH)2D3 pretreatment significantly alleviated the toxicity effects of Cd on the differentiation, apoptosis and extracellular matrix gene expression in primary chondrocytes. Conclusively, Cd exposure could inhibited chicken embryo chondrocytes differentiation, extracellular matrix gene expression, and induced chondrocyte apoptosis. However, these toxic effects of Cd are alleviated by the pretreatment of chondrocytes with 1α,25-(OH)2D3.

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LC–MS/MS determination of N‐acetyl‐l‐cysteine in chicken plasma

Roydeva,

Milanova

2024

Biomedical Chromatography

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N‐acetyl‐l‐cysteine (NAC) shows beneficial effects in cases of aflatoxicosis and heat stress in poultry but little is known about its pharmacokinetics in chickens. Therefore, the study aimed to develop and validate a sensitive LC–MS/MS analytical method for quantitative analysis of NAC in chicken plasma. A split calibration curve approach was used for determination of NAC in chicken plasma. Standard curves for low (0.05–2.5 μg/ml) and high (2.5–100 μg/ml) ranges of concentrations were prepared. The standard curves for low (r2 = 0.9987) and high (r2 = 0.9899) concentrations were linear within the tested range. The limits of detection (LOD) and of quantification (LOQ) for the standard at low concentrations were 0.093 and 0.28 μg/ml, respectively. The accuracy was from 97.35 to 101.33%. The values of LOD and LOQ for the standard at high concentrations were 0.76 and 2.30 μg/ml, respectively. The accuracy was between 99.77 and 112.14%. The intra‐ and inter‐day precisions for all concentrations from both standards did not exceed 8.57% and 10.69%, respectively. The recovery for all concentrations was between 92.45 and 105.52%. The validated method for determination of NAC in chicken plasma can be applied in future pharmacokinetic studies in chickens without dilution of samples and their repeated analysis.

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Antagonistic effect of N-acetyl-L-cysteine against cadmium-induced cytotoxicity and abnormal immune response on chicken peritoneal macrophages

Cited by 19 publications

References 58 publications

Effects of Cadmium Exposure on the Immune System and Immunoregulation

Effects of Cadmium Exposure on the Immune System and Immunoregulation

Cadmium Toxicity on Chondrocytes and the Palliative Effects of 1α, 25-Dihydroxy Vitamin D3 in White Leghorns Chicken's Embryo

LC–MS/MS determination of N‐acetyl‐l‐cysteine in chicken plasma

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