The Role of Nitric Oxide Synthase in an Early Phase Cd-Induced Acute Cytotoxicity in MCF-7 Cells

Zhong, Lingying; Wang, Lumei; Xu, Lurong; Liu, Qunlu; Jiang, Linlei; Zhi, Yuee; Lü, Wei; Zhou, Pei

doi:10.1007/s12011-014-0187-1

Cited by 14 publications

(7 citation statements)

References 32 publications

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“…It is speculated that it may be related to the excessive accumulation of free radicals in the body caused by Cd exposure ( Jihen el et al, 2009 ). Cd could regulate the body’s enzymatic activity to induce the accumulation of ROS ( Zhong et al, 2015 ), leading to oxidative damage ( Zhu et al, 2020 ), which in turn leads to pathological changes in the morphological structure of kidney tissue. Que is an effective scavenger of ROS and RNS.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of quercetin on cadmium-induced renal apoptosis through cyt-c/caspase-9/caspase-3 signaling pathway

Huang

Ding

et al. 2022

Front. Pharmacol.

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Cadmium (Cd), a heavy metal, has harmful effects on animal and human health, and it can also obviously induce cell apoptosis. Quercetin (Que) is a flavonoid compound with antioxidant and other biological activities. To investigate the protective effect of Que on Cd-induced renal apoptosis in rats. 24 male SD rats were randomly divided into four groups. They were treated as follows: control group was administered orally with normal saline (10 ml/kg); Cd group was injected with 2 mg/kg CdCl2 intraperitoneally; Cd + Que group was injected with 2 mg/kg CdCl2 and intragastric administration of Que (100 mg/kg); Que group was administered orally with Que (100 mg/kg). The experimental results showed that the body weight of Cd-exposed rats significantly decreased and the kidney coefficient increased. In addition, Cd significantly increased the contents of Blood Urea Nitrogen, Creatinine and Uric acid. Cd also increased the glutathione and malondialdehyde contents in renal tissues. The pathological section showed that Cd can cause pathological damages such as narrow lumen and renal interstitial congestion. Cd-induced apoptosis of kidney, which could activate the mRNA and protein expression levels of Cyt-c, Caspase-9 and Caspase-3 were significantly increased. Conversely, Que significantly reduces kidney damage caused by Cd. Kidney pathological damage was alleviated by Que. Que inhibited Cd-induced apoptosis and decreased Cyt-c, Caspase-9 and Caspase-3 proteins and mRNA expression levels. To sum up, Cd can induce kidney injury and apoptosis of renal cells, while Que can reduce Cd-induced kidney damage by reducing oxidative stress and inhibiting apoptosis. These results provide a theoretical basis for the clinical application of Que in the prevention and treatment of cadmium poisoning.

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Section: Discussionmentioning

confidence: 99%

Protective effect of quercetin on cadmium-induced renal apoptosis through cyt-c/caspase-9/caspase-3 signaling pathway

Huang

Ding

et al. 2022

Front. Pharmacol.

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“…Cd, as a transition element, cannot generate ROS directly. However, Cd could induce the accumulation of ROS by modulating the activities of various enzymes, such as nitric oxide synthase ( Zhong et al., 2015 ), which leads to oxidative damage that in turn leads to pathological changes of cellular structure and functions ( Huo et al., 2017 ). In the present study, many severe pathological changes and inflammatory responses with the increases dosage of Cd addition were reflected in the liver pathological slices, such as periportal fibrosis, bile duct hyperplasia, and inflammatory cells infiltrated around the hepatic central vein.…”

Section: Discussionmentioning

confidence: 99%

Histological changes, lipid metabolism, and oxidative and endoplasmic reticulum stress in the liver of laying hens exposed to cadmium concentrations

Zhu

Bai

et al. 2020

Poultry Science

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The objective of this study was to determine the effects of cadmium ( Cd ) on histological changes, lipid metabolism, and oxidative and endoplasmic reticulum ( ER ) stress in the liver of layers. A total of 480 hens at 38 wk of age were randomly assigned in 5 groups that were fed a basal diet or basal diet supplemented with CdCl 2 2.5H 2 O at 7.5, 15, 30, and 60 mg Cd/kg feed for 9 wk. The results showed that accumulation of Cd was the greatest in the kidney, followed by the liver, pancreas, and lung. Diet contaminated with 30 mg Cd/kg induced antioxidant defenses accompanied by the increase of the activities of antioxidant enzymes in the liver, while dietary supplementation with 60 mg Cd/kg decreased the antioxidant levels significantly ( P < 0.05). Immunofluorescence assay showed Cd induced reactive oxygen species production and endoplasmic reticulum stress in hepatocytes. Exposure to 60 mg Cd/kg significantly upregulated the expression of cytochrome C, caspase 3, caspase 9, caspase 7, Grp78, and Chop ( P < 0.05). Histopathology and quantitative real-time PCR results presented periportal fibrosis, bile duct hyperplasia, and periportal inflammatory cell infiltration in the liver accompanied by upregulating the expression of tumor necrosis factor-α, IL-6 and IL-10 in the 30- or 60-mg Cd/kg groups. Oil Red O staining and RT-qPCR results showed dietary supplementation with 7.5, 15, and 30 mg Cd/kg promoted the synthesis of lipid droplets and upregulated the expression of fatty acid synthase, while dietary supplementation with 60 mg Cd/kg attenuated the synthesis of lipid droplets and downregulated the expression of acyl-CoA oxidase 1, carnitine palmitoyltransferase-1, and perixisome proliferation-activated receptor α ( P < 0.05). Besides, the expression of vitellogenin ( VTG ) II and microsomal triglyceride transfer protein were upregulated in the 7.5-mg Cd/kg group, and the expressions of apolipoprotein B, vitellogenin II, and apolipoprotein very-low-density lipoprotein-II were downregulated in the 30- and/or 60-mg Cd/kg groups ( P < 0.05). Conclusively, although low-dose Cd exposure promoted the synthesis of lipids and lipoproteins in the liver, the increase of Cd exposure could trigger liver injury through inducing oxidative and endoplasmic reticulum stress and negatively affect lipid metabolism and yolk formation in laying hens.

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“…Zhong et al reported the ROS level in cells was increased after CdCl 2 exposure. It was demonstrated that NOS played a critical role on the Cd-induced ROS generation [22]. Cd 2+ also damages mitochondria which results in a disturbance of respiratory activity, alteration of inner membrane permeability, loss of membrane potential, swelling, activation of caspases and apoptosis, induction of mtDNA mutations and alteration of gene expression, as well as the induction of ROS [23].…”

Section: Discussionmentioning

confidence: 99%

The Co-induced Effects of Molybdenum and Cadmium on Antioxidants and Heat Shock Proteins in Duck Kidneys

Xia

Luo

Liu

et al. 2015

Biol Trace Elem Res

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Molybdenum (Mo) is an essential element for human beings and animals; however, high dietary intake of Mo can lead to adverse reactions. Cadmium (Cd) is harmful to health. To investigate the toxicity of Mo combined with Cd in duck kidneys, 240 ducks were randomly divided into six groups and treated with a commercial diet containing Mo, Cd or Mo combined with Cd. Kidneys were collected on days 30, 60, 90 and 120 for determining the expression of heat shock proteins (HSPs), including HSP60, HSP70 and HSP90 in the kidney through quantitative RT-PCR. We also determined the antioxidant activity indexes in the kidney mitochondria. Moreover, kidney tissues at 120 days were subjected to histopathological analysis with the optical microscope. The results indicated that the expression of HSPs was highly significantly (P <0.01) upregulated in the kidneys of the combination groups and the Cd group. Exposure to Cd and a high dose of Mo decreased the total antioxidative capacity and the activity of xanthine oxidase, while malondialdehyde levels and the activity of nitric oxide synthase increased compared with those of the control groups in the kidney mitochondria. This was particularly evident at 90 and 120 days. Histopathological lesions included congestion and bleeding in the renal interstitium, swelling of the distal convoluted tubule epithelial cells, granular degeneration and blister degeneration in the renal tubular epithelial cells. These results suggest that a combination of Mo and Cd leads to greater tissue damage and has a synergistic effect on kidney damage. Oxidative damage of kidney mitochondria may be a potential nephrotoxicity mechanism of molybdenum and cadmium, and the high expression of HSPs may play a role in the resistance of kidney toxicity induced by Mo and Cd.

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The Role of Nitric Oxide Synthase in an Early Phase Cd-Induced Acute Cytotoxicity in MCF-7 Cells

Cited by 14 publications

References 32 publications

Protective effect of quercetin on cadmium-induced renal apoptosis through cyt-c/caspase-9/caspase-3 signaling pathway

Protective effect of quercetin on cadmium-induced renal apoptosis through cyt-c/caspase-9/caspase-3 signaling pathway

Histological changes, lipid metabolism, and oxidative and endoplasmic reticulum stress in the liver of laying hens exposed to cadmium concentrations

The Co-induced Effects of Molybdenum and Cadmium on Antioxidants and Heat Shock Proteins in Duck Kidneys

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