ATOX1

Last update 08 May 2025

Basic Info

Synonyms

antioxidant 1 copper chaperone, ATOX1, Copper transport protein ATOX1

+ [2]

Introduction

Binds and deliver cytosolic copper to the copper ATPase proteins. May be important in cellular antioxidant defense.

100 Clinical Results associated with ATOX1

100 Translational Medicine associated with ATOX1

0 Patents (Medical) associated with ATOX1

339

Literatures (Medical) associated with ATOX1

01 Nov 2025·Neural Regeneration Research

Copper homeostasis and neurodegenerative diseases

Article

Author: Wang, Yuanyuan ; Li, Daidi ; Xu, Kaifei ; Zhang, Feng ; Wang, Guoqing

Copper, one of the most prolific transition metals in the body, is required for normal brain physiological activity and allows various functions to work normally through its range of concentrations. Copper homeostasis is meticulously maintained through a complex network of copper-dependent proteins, including copper transporters (CTR1 and CTR2), the two copper ion transporters the Cu -transporting ATPase 1 (ATP7A) and Cu-transporting beta (ATP7B), and the three copper chaperones ATOX1, CCS, and COX17. Disruptions in copper homeostasis can lead to either the deficiency or accumulation of copper in brain tissue. Emerging evidence suggests that abnormal copper metabolism or copper binding to various proteins, including ceruloplasmin and metallothionein, is involved in the pathogenesis of neurodegenerative disorders. However, the exact mechanisms underlying these processes are not known. Copper is a potent oxidant that increases reactive oxygen species production and promotes oxidative stress. Elevated reactive oxygen species levels may further compromise mitochondrial integrity and cause mitochondrial dysfunction. Reactive oxygen species serve as key signaling molecules in copper-induced neuroinflammation, with elevated levels activating several critical inflammatory pathways. Additionally, copper can bind aberrantly to several neuronal proteins, including alpha-synuclein, tau, superoxide dismutase 1, and huntingtin, thereby inducing neurotoxicity and ultimately cell death. This study focuses on the latest literature evaluating the role of copper in neurodegenerative diseases, with a particular focus on copper-containing metalloenzymes and copper-binding proteins in the regulation of copper homeostasis and their involvement in neurodegenerative disease pathogenesis. By synthesizing the current findings on the functions of copper in oxidative stress, neuroinflammation, mitochondrial dysfunction, and protein misfolding, we aim to elucidate the mechanisms by which copper contributes to a wide range of hereditary and neuronal disorders, such as Wilson’s disease, Menkes’ disease, Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and multiple sclerosis. Potential clinically significant therapeutic targets, including superoxide dismutase 1, D-penicillamine, and 5,7-dichloro-2-[(dimethylamino)methyl]-8-hydroxyquinoline, along with their associated therapeutic agents, are further discussed. Ultimately, we collate evidence that copper homeostasis may function in the underlying etiology of several neurodegenerative diseases and offer novel insights into the potential prevention and treatment of these diseases based on copper homeostasis.

01 Apr 2025·Journal of Hazardous Materials

Combined exposure to microplastics and copper elicited size-dependent uptake and toxicity responses in red swamp crayfish (Procambarus clarkia)

Article

Author: Wei, Wei ; Zeng, Huixin ; Zhong, Yanfei ; Xu, Xiaoli ; Luo, Mingzhong

In recent years, the toxicity of microplastics (MPs) in combination with heavy metals, particularly the influence of varying microplastic sizes on their toxic effects, has attracted widespread attention. In this study, red swamp crayfish (Procambarus clarkia) were exposed to MPs of two particle sizes (S-MPs: 5 μm, 1 mg/L; and L-MPs: 100 μm, 1 mg/L) and Cu (5 mg/L) individually or in combination for 96 h. The accumulation patterns of MPs were as follows: gills > intestines > hepatopancreas > muscles. Moreover, the accumulation pattern of Cu was as follows: intestines > gills > hepatopancreas > muscle. Additionally, S-MPs and L-MPs enhanced Cu accumulation, with the highest levels observed in the S-MPs+Cu-treated group. Histopathological analysis showed that the combined exposure led to greater hepatopancreatic damage. Assessment of antioxidant enzymes showed decreased activities of superoxide dismutase, catalase, and glutathione among the different treatments, except for malondialdehyde, which was elevated compared to the control group. In the S-MPs+Cu-treated group, the expression levels of Cu homeostasis genes (MTF-1, ATP2, Atox1, MT) were significantly lower than those in the Cu treated group. This study provides a valuable reference for studying the combined toxic effects of MPs with varying particle sizes on heavy metals.

01 Mar 2025·Biological Trace Element Research

Effects of Perioperative Zinc Supplementation on Copper Circulating Levels and Expression of Metallothionein and Copper Antioxidant Chaperone-1 in Leukocytes in Patients Undergoing CABG Surgery

Article

Author: Nakhaeizadeh, Reza ; Shahparvari, Mohammad Reza ; Nasrollahzadeh, Javad ; Roohelhami, Elham ; Makiabadi, Elham

The use of zinc supplement may have a negative effect on copper status. The objective of this study was to evaluate the effect of zinc and vitamin E supplementation on copper and zinc biomarkers in patients undergoing coronary artery bypass graft (CABG) surgery. The study was an add-on project to a previously published randomized controlled trial (NCT05402826) on patients undergoing CABG surgery. Patients in the zinc-vitamin E group (n = 40) received oral zinc (120 mg) and vitamin E (1200 international units) 1 day before surgery, followed by 30 mg of zinc and 200 units of vitamin E per day until 21 days after surgery, while those in the control group (n = 38) received placebo. Plasma levels of copper, ceruloplasmin, superoxide dismutase (SOD) activity, as well as leukocyte gene expression of metallothionein 2A (MT2A) and antioxidant protein 1 (ATOX1), were determined 3 and 21 days after surgery. The plasma copper level in the zinc-vitamin E group was significantly lower than the placebo group on the 3rd postoperative day, but no significant between-group differences were observed on day 21. Plasma ceruloplasmin concentration and SOD activity were not different. Relative mRNA expression of leukocyte MT2A was increased at both times (days 3 and 21 in the zinc-vitamin E group compared to placebo, but ATOX1 expression was not affected. Although the plasma copper level was transiently decreased early after surgery in the zinc-vitamin E group, considering the lack of change in other copper biomarkers, it seems that the use of zinc supplements at the dose used in the present study does not have a significant negative effect on the role of intracellular copper.

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ATOX1

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