Cytotoxicity effect of nickel hydroxide nanoparticles functionalized by glutamine and conjugated by thiosemicarbazide on human lung cancer cell line (A549) and evaluation of bax and bcl-2 genes expression

Dehkaei, Artadokht Aghaeipour; Khalatbari, Kimia; Emamifar, Alireza; Taramsari, Somayeh Maghsoomi; Balkhi, Sahar; Ghezeljeh, Somayeh Mikaeili; Gorji, Selena; Gholipoor, Sevda; Noveiri, Mahboubeh Jahani Sayyad; Hedayati, Mohammad; Salehzadeh, Ali

doi:10.1016/j.genrep.2022.101700

Cited by 4 publications

(2 citation statements)

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“…Levels of NiCl 2 in food exceeding 300 mg/kg induce oxidative stress and inflammation of the lungs in broiler chickens, leading to pathological lung damage and impaired respiratory function 8 . Ni and Ni compounds can affect various metabolic pathways in cells and influence processes including apoptosis, autophagy, invasion, metastasis, and proliferation, and may consequently promote the development of lung cancer 9–12 …”

Section: Introductionmentioning

confidence: 99%

“…8 Ni and Ni compounds can affect various metabolic pathways in cells and influence processes including apoptosis, autophagy, invasion, metastasis, and proliferation, and may consequently promote the development of lung cancer. [9][10][11][12] PF is a chronic lung disease, characterized by the overaccumulation of fibroblasts, abnormal collagen deposition in extracellular matrices, and disruption of alveolar structure, thereby decreasing lung compliance and eventually resulting in pulmonary dysfunction.…”

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confidence: 99%

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Nickel induces epithelial‐mesenchymal transition in pulmonary fibrosis in mice via activation of the oxidative stress‐mediated TGF‐β1/Smad signaling pathway

Cao,

Yin,

et al. 2024

Environmental Toxicology

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Nickel (Ni) is recognized as a carcinogenic metal, and its widespread use has led to severe environmental and health problems. Although the lung is among the main organs affected by Ni, the precise mechanisms behind this effect remain poorly understood. This study aimed to elucidate the physiological mechanisms underlying Ni‐induced pulmonary fibrosis (PF), using various techniques including histopathological detection, biochemical analysis, immunohistochemistry, western blotting, and quantitative real‐time PCR. Mice were treated with nickel chloride (NiCl2), which induced PF (detected by Masson staining), up‐regulation of α‐smooth muscle actin (α‐SMA), and collagen‐1 mRNA and protein expression. NiCl2 was found to induce PF by: activation of the epithelial‐mesenchymal transition (EMT) and the transforming growth factor‐β1 (TGF‐β1)/Smad signaling pathway; up‐regulation of protein and mRNA expression of TGF‐β1, p‐Smad2, p‐Smad3, vimentin, and N‐cadherin; and down‐regulation of protein and mRNA expression of E‐cadherin. In addition, NiCl2 treatment increased malondialdehyde content while inhibiting antioxidant activity, as indicated by decreased catalase, total antioxidant capacity, and superoxide dismutase activities, and glutathione content. Co‐treatment with the effective antioxidant and free radical scavenger N‐acetyl cysteine (NAC) plus NiCl2 was used to study the effects of oxidative stress in NiCl2‐induced PF. The addition of NAC significantly mitigated NiCl2‐induced PF, and reversed activation of the TGF‐β1/Smad signaling pathway and EMT. NiCl2‐induced PF was therefore shown to be due to EMT activation via the TGF‐β1/Smad signaling pathway, mediated by oxidative stress.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%