Copper-induced apoptosis and autophagy through oxidative stress-mediated mitochondrial dysfunction in male germ cells

Kang, Zhenlong; Qiao, Na; Liu, Gaoyang; Chen, Hanming; Tang, Zhaoxin; Liu, Ying

doi:10.1016/j.tiv.2019.104639

Cited by 69 publications

(37 citation statements)

References 49 publications

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“…Infrasound exposure destroyed oxidation-antioxidant balance and increased lipofuscin accumulation in neurons of the mouse brain cortex [19]. Oxidative stress can induce apoptosis [20], and the apoptosis may result in the loss of postsynaptic proteins [21]. Postsynaptic current was modulated by postsynaptic proteins [22] while postsynaptic neurons modulate learning [23] and their dysfunction will impair memory [24].…”

Section: Introductionmentioning

confidence: 99%

Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity

Zhou

Yang

Fan

et al. 2020

Oxidative Medicine and Cellular Longevity

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Background. Infrasound is a major threat to global health by causing injuries of the central nervous system (CNS). However, there remains no effective therapeutic agent for preventing infrasound-caused CNS injury. 2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glycoside (THSG) exerts protective function against CNS injuries and may have beneficial effects on infrasound-induced CNS impairment. Methods. A mouse model with CNS (oxidative stress-induced inflammation and neuronal apoptosis) injuries was established when the mouse was exposed to the infrasound of 16 Hz at 130 dB for 2 h each day and the duration of treatment was 8 d. The mice were divided into the control (CG, healthy mice), the model (MG, model mice), and the THSG (EG, experimental group, model mice treated with THSG) groups. The learning and memory impairments caused by infrasound were examined using a Morris water maze test. Lipid profiles, antioxidant biomarkers, and inflammatory cytokines in hippocampus tissue were measured by using corresponding ELISA kits. Meanwhile, BCL-2/BAX/caspase-3 signaling pathway was measured in the hippocampi and prefrontal cortex of the mouse brain using real-time qPCR and Western blot. Nissl’s stain was used to measure neuronal necrosis in the hippocampi and prefrontal cortex of the mouse brain. Results. THSG significantly ameliorated the learning and memory impairments caused by infrasound. On the other hand, THSG improved lipid profiles, increased antioxidant properties by affecting the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA), and displayed anti-inflammatory action via the downregulation of IL- (interleukin-) 6, IL-8, IL-10, TNF- (tumor necrosis factor-) α, and hs-CRP (high-sensitivity C-reactive protein) in the hippocampal tissues of the mouse model (P<0.05). Additionally, Nissl’s stain showed that THSG inhibited infrasound-induced neuronal necrosis in the hippocampi and prefrontal cortex. Besides, THSG exerted antiapoptosis function by upregulating the level of Bcl-2 and downregulating the levels of BAX and caspase-3 in the hippocampi. Conclusion. THSG may be an effective anti-infrasound drug against CNS injury by improving antioxidant, anti-inflammatory, antiapoptosis, and antinecrosis capacities. Further research is still needed to confirm the exact molecular mechanism.

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Section: Introductionmentioning

confidence: 99%

Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity

Zhou

Yang

Fan

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…11 Mitochondrial dysfunction is caused by the extensive OS as the mitochondrial transmembrane potential and ATP levels decrease, which finally results in the apoptosis of cells. 12 To protect vascular endothelial cells from the damage of harmful stimulators and decrease the risk of arterial stiffness, alleviating the apoptosis caused by extensive OS might be an effective therapeutic method.…”

Section: Introductionmentioning

confidence: 99%

<p>Loxoprofen Sodium Alleviates Oxidative Stress and Apoptosis Induced by Angiotensin II in Human Umbilical Vein Endothelial Cells (HUVECs)</p>

Ji¹,

Yu²,

Zhang³

et al. 2020

DDDT

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“…CytC in the cytosol also leads to apoptosome formation, which triggers caspase-9 and caspase-3-mediated apoptosis [ 43 ]. It has been demonstrated that CuSO 4 treatment significantly up-regulated the expression of Bax, CytC, caspase-9, and caspase-3 mRNAs and proteins followed to cause the cell apoptosis in chicken hepatocytes and male germ cells [ 44 , 45 ]. Rapamycin can partly inhibit mitochondria dysfunction (e.g., up-regulate the adenosine triphosphate (ATP) levels, mitochondrial mass, and mitochondria membrane potential) and attenuate CuSO4-induced cell apoptosis in chicken hepatocytes in vitro [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…Copper can accumulate in the liver, kidney and brain tissues, and it is up to 17.5 μg/g kidney (wet weight) (it is equal to about 270 μM) when rats were orally administered with 200 mg/kg/day for 30 days [ 11 ]. The literature suggested that CuSO 4 exposure at the doses of 50–1000 μM exhibited cytotoxicity in the male germ cells indicated, chicken hepatocytes, and human Caco-2 and HepG2 cells in vitro [ 45 , 47 , 48 ]. In the present study, CuSO 4 treatment at 50–400 μM for 24 h significantly decreased the cell viability of HEK293 cells in a dose-dependent manner ( Figure 5 ).…”

Section: Discussionmentioning

confidence: 99%

Molecular Insights of Copper Sulfate Exposure-Induced Nephrotoxicity: Involvement of Oxidative and Endoplasmic Reticulum Stress Pathways

Dai

Liu

et al. 2020

Biomolecules

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The precise pathogenic mechanism in Cu exposure-cause nephrotoxicity remains unclear. This study investigated the underlying molecular mechanism of copper sulfate (CuSO4)-induced nephrotoxicity. Mice were treated with CuSO4 at 50, 100, 200 mg/kg/day or co-treated with CuSO4 (200 mg/kg/day) and 4-phenylbutyric acid (4-PBA, 100 mg/kg/day) for 28 consecutive days. HEK293 cells were treated with CuSO4 (400 μM) with or without superoxide dismutase, catalase or 4-PBA for 24 h. Results showed that CuSO4 exposure can cause renal dysfunction and tubular necrosis in the kidney tissues of mice. CuSO4 exposure up-regulated the activities and mRNA expression of caspases-9 and -3 as well as the expression of glucose-regulated protein 78 (GRP78), GRP94, DNA damage-inducible gene 153 (GADD153/CHOP), caspase-12 mRNAs in the kidney tissues. Furthermore, superoxide dismutase and catalase pre-treatments partly inhibited CuSO4-induced cytotoxicity by decreasing reactive oxygen species (ROS) production, activities of caspases-9 and -3 and DNA fragmentations in HEK293 cells. 4-PBA co-treatment significantly improved CuSO4-induced cytotoxicity in HEK293 cells and inhibited CuSO4 exposure-induced renal dysfunction and pathology damage in the kidney tissues. In conclusion, our results reveal that oxidative stress and endoplasmic reticulum stress contribute to CuSO4-induced nephrotoxicity. Our study highlights that targeting endoplasmic reticulum and oxidative stress may offer an approach for Cu overload-caused nephrotoxicity.

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Copper-induced apoptosis and autophagy through oxidative stress-mediated mitochondrial dysfunction in male germ cells

Cited by 69 publications

References 49 publications

Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity

Tetrahydroxystilbene Glucoside Ameliorates Infrasound-Induced Central Nervous System (CNS) Injury by Improving Antioxidant and Anti-Inflammatory Capacity

<p>Loxoprofen Sodium Alleviates Oxidative Stress and Apoptosis Induced by Angiotensin II in Human Umbilical Vein Endothelial Cells (HUVECs)</p>

Molecular Insights of Copper Sulfate Exposure-Induced Nephrotoxicity: Involvement of Oxidative and Endoplasmic Reticulum Stress Pathways

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