Chlorpyrifos induced autophagy and mitophagy in common carp livers through AMPK pathway activated by energy metabolism disorder

Cui, Jiawen; Hao, Zhiyu; Zhou, Qin; Qiu, Minna; Liu, Yuhang; Wang, Kun; Teng, Xiaohua; Lu, Kang

doi:10.1016/j.ecoenv.2023.114983

Cited by 27 publications

(9 citation statements)

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“…Three reports are in concordance with our findings. Oxidative stress occurred with increased MDA and decreased GSH in the livers of chlorpyrifos-treated common carps [ 49 ], as well as in the cerebral cortex of Pb-treated rats [ 36 ]. Pancreatic oxidative stress occurred in bisphenol A-exposed chickens with up-regulated MDA and down-regulated GSH and TAC [ 8 ].…”

Section: Discussionmentioning

confidence: 99%

Se Alleviated Pb-Caused Neurotoxicity in Chickens: SPS2-GPx1-GSH-IL-2/IL-17-NO Pathway, Selenoprotein Suppression, Oxidative Stress, and Inflammatory Injury

Li,

Liang,

Jiang

et al. 2024

Antioxidants

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Lead (Pb), a heavy metal environmental pollutant, poses a threat to the health of humans and birds. Inflammation is one of the most common pathological phenomena in the case of illness and poisoning. However, the underlying mechanisms of inflammation remain unclear. The cerebellum and the thalamus are important parts of the nervous system. To date, there have been no reports of Pb inducing inflammation in animal cerebellums or thalami. Selenium (Se) can relieve Pb poisoning. Therefore, we aimed to explore the mechanism by which Se alleviates Pb toxicity to the cerebellums and thalami of chickens by establishing a chicken Pb or/and Se treatment model. Our results demonstrated that exposure to Pb caused inflammatory damage in cerebellums and thalami, evidenced by the characteristics of inflammation, the decrease in anti-inflammatory factors (interleukin (IL)-2 and interferon-γ (INF-γ)), and the increase in pro-inflammatory factors (IL-4, IL-6, IL-12β, IL-17, and nitric oxide (NO)). Moreover, we found that the IL-2/IL-17–NO pathway took part in Pb-caused inflammatory injury. The above findings were reversed by the supplementation of dietary Se, meaning that Se relieved inflammatory damage caused by Pb via the IL-2/IL-17–NO pathway. In addition, an up-regulated oxidative index malondialdehyde (MDA) and two down-regulated antioxidant indices (glutathione (GSH) and total antioxidant capacity (TAC)) were recorded after the chickens received Pb stimulation, indicating that excess Pb caused an oxidant/antioxidant imbalance and oxidative stress, and the oxidative stress mediated inflammatory damage via the GSH–IL-2 axis. Interestingly, exposure to Pb inhibited four glutathione peroxidase (GPx) family members (GPx1, GPx2, GPx3, and GPx4), three deiodinase (Dio) family members (Dio1, Dio2, and Dio3), and fifteen other selenoproteins (selenophosphate synthetase 2 (SPS2), selenoprotein (Sel)H, SelI, SelK, SelM, SelO, SelP1, SelPb, SelS, SelT, SelU, and selenoprotein (Sep)n1, Sepw1, Sepx1, and Sep15), suggesting that Pb reduced antioxidant capacity and resulted in oxidative stress involving the SPS2–GPx1–GSH pathway. Se supplementation, as expected, reversed the changes mentioned above, indicating that Se supplementation improved antioxidant capacity and mitigated oxidative stress in chickens. For the first time, we discovered that the SPS2–GPx1–GSH–IL-2/IL-17–NO pathway is involved in the complex inflammatory damage mechanism caused by Pb in chickens. In conclusion, this study demonstrated that Se relieved Pb-induced oxidative stress and inflammatory damage via the SPS2–GPx1–GSH–IL-2/IL-17–NO pathway in the chicken nervous system. This study offers novel insights into environmental pollutant-caused animal poisoning and provides a novel theoretical basis for the detoxification effect of Se against oxidative stress and inflammation caused by toxic pollutants.

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Section: Discussionmentioning

confidence: 99%

Se Alleviated Pb-Caused Neurotoxicity in Chickens: SPS2-GPx1-GSH-IL-2/IL-17-NO Pathway, Selenoprotein Suppression, Oxidative Stress, and Inflammatory Injury

Li,

Liang,

Jiang

et al. 2024

Antioxidants

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“…The ethanol standard for the control group was composed of 10 mL of ethanol and 490 mL of double-distilled water. The ethanol concentration of every control tank was generated through the combination of 4 mL of a standard solution with 5 L of double-distilled water [9].…”

Section: Chemicalsmentioning

confidence: 99%

“…All physiochemical parameters were monitored to keep fish in groups 1 (control), 2 (low dosage metformin 40 µg/L), and 3 (high dose metformin 80 µg/L) at a consistent level [14]. Animals had their water replaced and were given a dose of metformin that was safe for the environment every day before noon [9]. The water was routinely changed throughout the experimentation to prevent the animals from exposure to water pollution and keep them stress free.…”

Section: Experimental Setup and Sample Collectionmentioning

confidence: 99%

“…In addition, the male testis of Pimephales promelas exposed to metformin exhibits the considerable induction of intersex after being treated with 40 µg/L metformin for one year. In addition, the common carp liver is a target organ attacked by the toxic environmental pollutants chlorpyrifos and 4-tert-butylphenol [9,10]. Excess environmental pollutants can cause oxidative stress [10,11] and immunosuppression [9].…”

Section: Introductionmentioning

confidence: 99%

“…In addition, the common carp liver is a target organ attacked by the toxic environmental pollutants chlorpyrifos and 4-tert-butylphenol [9,10]. Excess environmental pollutants can cause oxidative stress [10,11] and immunosuppression [9]. Oxidative stress and immunity are involved in the molecular mechanism in Luciobarbus capito (L. capito) under a high-salinity environment [12].…”

Section: Introductionmentioning

confidence: 99%

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Biochemical Patterns and Genotoxicity of the Endocrine Disruptor Metformin in the Freshwater Fish Labeo rohita

Sibiya

Al‐Ghanim

Govindarajan

et al. 2023

Fishes

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Metformin is one of the most extensively used drugs, making it one of the most likely endocrine disruptors in the environment, which may negatively affect fish and other freshwater animals. Still, there is a dearth of studies examining metformin’s impact on freshwater creatures, like fish. This research aimed to identify the biochemical and genotoxicity effects of the endocrine disruptor metformin in the freshwater fish Labeo rohita at ecologically appropriate doses. Metformin’s toxicity was evaluated by subjecting L. rohita to the drug over 28 days at two dosages (40 µg/L to 80 µg/L). The results indicated that 40 µg/L and 80 µg/L of metformin caused an increase in reactive oxygen species and the generation of free radicals in the body of L. rohita, which in turn caused impairment and alterations in total hemoglobin, red blood corpuscles, white blood corpuscles, oxidative stress, lipid peroxidation, protein carbonyl activity, respiratory burst activity, myeloperoxidase activity, and lysozyme activity. In addition, animals treated with the maximum metformin dose (80 µg/L) demonstrated substantial DNA damage in the genotoxicity experiment. Metformin’s endocrine-disrupting actions may have unintended ramifications for the well-being of aquatic species in their natural habitats. Results of the study demonstrated a serious concern that metformin exposure might be harmful to aquatic life.

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Capsaicin reverses cisplatin resistance in tongue squamous cell carcinoma by inhibiting the Warburg effect and facilitating mitochondrial‐dependent apoptosis via the AMPK/AKT/mTOR axis

Liu,

Li,

Zhao

et al. 2024

Cell Biology International

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Cisplatin is commonly used for the chemotherapy of tongue squamous cell carcinoma (TSCC); however, adverse side effects and drug resistance impact its therapeutic efficacy. Capsaicin is an active ingredient in chili peppers that exerts antitumor effects, whether it exerts antitumor effects on cisplatin‐resistant cells remains unknown. Therefore, in this study, we investigated the effect of capsaicin on cisplatin resistance in TSCC cells and explored the underlying mechanisms. A cisplatin‐resistant TSCC cell line was established by treated with increasing cisplatin concentrations. Combined treatment with cisplatin and capsaicin decreased the glucose consumption and lactate dehydrogenase activity and increased the adenosine triphosphate production both in vitro and in vivo, suggesting the inhibition of the Warburg effect. Moreover, this combined treatment induced cell apoptosis and significantly upregulated the levels of proapoptotic proteins, such as Bax, cleaved caspase‐3, ‐7, and ‐9, and apoptosis‐inducing factor. In contrast, levels of the antiapoptotic protein, Bcl‐2, were downregulated. Additionally, LKB1 and AMPK activities were stimulated, whereas those of AKT and mTOR were suppressed. Notably, AMPK knockdown abolished the inhibitory effects of capsaicin and cisplatin on the AKT/mTOR signaling pathway and Warburg effect. Overall, combined treatment with capsaicin and cisplatin reversed cisplatin resistance by inhibiting the Warburg effect and facilitating mitochondrial‐dependent apoptosis via the AMPK/AKT/mTOR axis. Our findings suggest combination therapy with capsaicin and cisplatin as a potentially novel strategy and highlight capsaicin as a promising adjuvant drug for TSCC treatment.

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Chlorpyrifos induced autophagy and mitophagy in common carp livers through AMPK pathway activated by energy metabolism disorder

Cited by 27 publications

References 50 publications

Se Alleviated Pb-Caused Neurotoxicity in Chickens: SPS2-GPx1-GSH-IL-2/IL-17-NO Pathway, Selenoprotein Suppression, Oxidative Stress, and Inflammatory Injury

Se Alleviated Pb-Caused Neurotoxicity in Chickens: SPS2-GPx1-GSH-IL-2/IL-17-NO Pathway, Selenoprotein Suppression, Oxidative Stress, and Inflammatory Injury

Biochemical Patterns and Genotoxicity of the Endocrine Disruptor Metformin in the Freshwater Fish Labeo rohita

Capsaicin reverses cisplatin resistance in tongue squamous cell carcinoma by inhibiting the Warburg effect and facilitating mitochondrial‐dependent apoptosis via the AMPK/AKT/mTOR axis

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