Nickel(II) oxide  (Synonyms: Nickel monoxide)

Nickel(II) oxide (nickel monoxide) is a chemical warfare agent that can enter the body through the respiratory tract and other routes, distributing to organs such as the lungs and testes. The nanoparticle form of nickel(II) oxide (NiO NPs) exhibits antibacterial, anti-leishmanial, anti-diabetic, and anti-cancer activities. NiO NPs can be activated by ultraviolet and visible light, generating reactive oxygen species (ROS). Nickel(II) oxide induces oxidative stress by generating reactive oxygen species, activating the TGF-β1-mediated MAPK and PI3K/AKT pathways, disrupting the MMPs/TIMPs balance, and upregulating the expression of inflammatory factors (IL-1β, IL-6) and apoptosis-related molecules (Bax, caspase-3, p53), while inhibiting the activity of the anti-apoptotic molecule Bcl-2. Nickel(II) oxide induces cytotoxicity, promotes fibrosis, triggers inflammatory responses, and causes apoptosis. Nickel(II) oxide can be applied in research on the safety assessment of nanomaterials, such as in the context of pulmonary fibrosis and reproductive system toxicity^[1][2][3].

Nickel(II) oxide (12.5, 25, 50, 100, 200 μg/mL; 24 h) reduced A549 cell viability in a dose-dependent manner and increased lactate dehydrogenase (LDH) activity in the culture medium, with cell viability maintained at 60%-80% at concentrations of 25, 50, and 100 μg/mL^[1].
Nickel(II) oxide (25, 50, 100 μg/mL; 24 h) dose-dependently increased hydroxyproline (Hyp) content and type I collagen (Col-I) protein expression in A549 cell culture medium, with significantly increased Hyp content in the 100 μg/mL group and upregulated Col-I expression in the 50 and 100 μg/mL groups^[1].
Nickel(II) oxide (25, 50, 100 μg/mL; 24 h) dose-dependently upregulated TGF-β1 protein expression in A549 cells, activating the p38 MAPK and ERK1/2 pathways, with increased gene and phosphorylated protein levels while total protein levels remained unchanged^[1].
Nickel(II) oxide (25, 50, 100 μg/mL; 24 h) induced MMPs/TIMPs imbalance in A549 cells, with significantly increased MMP-9 gene and protein levels in the 50 and 100 μg/mL groups, dose-dependent upregulation of TIMP-1 and TIMP-2, and increased MMP-2 protein expression only in the 100 μg/mL group^[1].
Nickel(II) oxide (100 μg/mL; pre-treatment with inhibitor for 1 hour followed by 24 h treatment) combined with 10 μM TGF-β1 inhibitor SB431542 (HY-10431) downregulated p-p38 MAPK and p-ERK1/2 levels in A549 cells and increased cell viability^[1].
Nickel(II) oxide (100 μg/mL; pre-treatment with inhibitor for 1 hour followed by 24 h treatment) in combination with 10 μM p38 inhibitor SB203580 (HY-10256) or ERK1/2 inhibitor U0126 (HY-12031A) reduced the protein levels of Col-I, MMP-2, MMP-9, TIMP-1, and TIMP-2^[1].
Nickel(II) oxide (25, 50, 100 μg/mL; 24 h) dose-dependently downregulated lncRNA MEG3 expression in A549 cells, with significant effects at 50 and 100 μg/mL, and simultaneously activated the PI3K/AKT pathway (increased p-PI3K, p-AKT, and p-mTOR)^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Nickel(II) oxide (0.015-0.24 mg/kg; intratracheal instillation; twice weekly; 9 weeks) in a pulmonary fibrosis model of male rats led to significant widening of alveolar septa, dose-dependent increase in hydroxyproline content in lung tissue, upregulation of TGF-β1 protein expression, activation of the PI3K/AKT signaling pathway, and downregulation of long non-coding RNA Meg3 expression^[2].
Nickel(II) oxide (micron-sized, 150 mg/kg; oral administration; once daily; 21 days) in a normal male rat model reduced the activity of acetylcholinesterase (AChE) and antioxidant enzymes (SOD, CAT, GPx, GST) in testicular tissue, increased levels of malondialdehyde (MDA), IL-1β, IL-6, and 8-OHdG, affected the expression of apoptotic markers, and caused degeneration of seminiferous tubules^[3].
Nickel(II) oxide (micron-sized, 20 mg/kg; intraperitoneal injection; once daily; 21 days) in a normal male rat model showed more significant testicular toxicity effects than the oral administration group, and also induced testicular interstitial edema and upregulated the expression of the endoplasmic reticulum stress marker GRP78^[3].
Nickel(II) oxide (micron-sized, 1 mg/kg; intravenous injection; once daily; 21 days) in a normal male rat model showed the strongest toxicity in the micron-sized administration group, with irregular indentations in the seminiferous tubules and higher levels of abnormality in various biochemical indicators compared to the oral and intraperitoneal injection groups^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

74.69

NiO

1313-99-1

Solid

Brown to breen

[Ni]=O

Room temperature in continental US; may vary elsewhere.

Store at room temperature, keep dry and cool

• [1]. Tian M, et al. TGF-β1 mediated MAPK signaling pathway promotes collagen formation induced by Nano NiO in A549 cells. Environ Toxicol. 2019 Jun;34(6):719-727.  [Content Brief]

  [2]. Zhan H, et al. LncRNA MEG3 Involved in NiO NPs-Induced Pulmonary Fibrosis via Regulating TGF-β1-Mediated PI3K/AKT Pathway. Toxicol Sci. 2021 Jul 16;182(1):120-131.  [Content Brief]

  [3]. Adiguzel C, et al. Biochemical, Immunohistochemical, Histopathological, and Apoptotic Evaluation of Nickel Oxide Nanoparticle- and Microparticle-Induced Testicular Toxicity in Male Rats. ACS Omega. 2024 Dec 18;9(52):50910-50921.  [Content Brief]