Arsenic Trioxide Exposure Induces Heat Shock Protein Responses in Cock Livers

Zhang, Kexin; Zhao, Panpan; Guo, Guangyang; Guo, Ying; Li, Siwen; He, Ying; Sun, Xiao; Chai, Hongliang; Zhang, Wen; Xing, Mingwei

doi:10.1007/s12011-015-0487-0

Cited by 5 publications

(3 citation statements)

References 38 publications

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“…As one of the major inducible HSPs, HSP70 is widely used as a heat stress marker in various studies (Morimoto 1993). Heat exposure can upregulate HSP70 in embryos (Skjaerven et al 2011;Sakatani et al 2012) and increase HSP27 in mammary gland (Li et al 2019), liver (Zhang et al 2016), and cardiac cells (Parida et al 2019). Similarly, our current study found that HSP70 was increased in both abdominal fat and liver and HSP27 was increased in the liver, indicating the adaptive response of these piglets in response to heat stress even when they were in utero of sows and during lactation period.…”

Section: Discussionmentioning

confidence: 99%

Maternal heat stress regulates the early fat deposition partly through modification of m6A RNA methylation in neonatal piglets

Heng

Tian

Zhang

et al. 2019

Cell Stress and Chaperones

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It is known that heat stress induces various physiological challenges in livestock production including changes in lipid metabolism. However, the molecular mechanism of how heat stress regulates lipid metabolism at the mRNA level is still largely unknown. N 6 -methyl-adenosine (m 6 A) is the most common and abundant modification on RNA molecules present in eukaryotes, which affects almost all aspects of RNA metabolism and thus gives us the hint that it may participate in changes of gene expression of lipid metabolism during heat stress. Therefore, the purpose of the present study was to investigate the effect of heat stress on fat metabolism in 21-day Large White × Landrace piglets from sows challenged by heat stress from day 85 of gestation until day 21 of lactation. We measured the expression of heat shock proteins (HSPs), genes associated with lipid metabolism, m 6 A-related enzymes, and m 6 A levels in abdominal fat and liver of offspring piglets. Our results showed that high ambient temperature significantly increased the expression of HSP70 (P < 0.01) in both liver and abdominal fat and upregulated HSP27 in the liver (P < 0.05). Additionally, genes involved in fat metabolism such as ACACA, FASN, DGAT1, PPAR-γ, SREBP-1c, and FABP4 were upregulated in abdominal fat in the experimental group challenged by high ambient temperature. In the liver, heat stress increased the mRNA expression of DGAT1, SREBP-1c, and CD36 and decreased ATGL and CPT1A expression (P < 0.05). The m 6 A level was higher in the heat stress group compared with the control group in the liver and abdominal fat of offspring piglets (P < 0.01). Notably, heat stress also increased gene expression of METTL14, WTAP, FTO, and YTHDF2 (P < 0.05) in both abdominal fat and liver. The protein abundances of METTL3, METTL14, and FTO were upregulated after heat stress in abdominal fat (P < 0.05) but not in the liver. Although there was no difference in the protein abundance of YTHDF2 in abdominal fat, its level was increased in the liver (P < 0.05). In conclusion, our findings showed that heat stress increased expression of genes involved in lipogenesis, which provided scientific evidence to the observation of increased fatness in pigs under heat stress. We also demonstrated a possible mechanism that m 6 A RNA modification may be associated with these changes in lipid metabolism upon heat stress.

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Section: Discussionmentioning

confidence: 99%

Maternal heat stress regulates the early fat deposition partly through modification of m6A RNA methylation in neonatal piglets

Heng

Tian

Zhang

et al. 2019

Cell Stress and Chaperones

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“…Molecular chaperones are a group of proteins that have functional similarity and modulate the proteostasis network by sensing and proofreading misfolded peptides to avoid aggregation [ 184 ]. It has been suggested that exposure to arsenic leads to the disruption of the functions of molecular chaperones [ 185 ]. As a division of the cellular stress response, inorganic arsenic (As 3+ ) was found to induce HSP70 and small HSP’s expression.…”

Section: Toxicological Pathwaysmentioning

confidence: 99%

Molecular Mechanism of Arsenic-Induced Neurotoxicity including Neuronal Dysfunctions

Thakur

Rachamalla

Niyogi

et al. 2021

IJMS

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Arsenic is a key environmental toxicant having significant impacts on human health. Millions of people in developing countries such as Bangladesh, Mexico, Taiwan, and India are affected by arsenic contamination through groundwater. Environmental contamination of arsenic leads to leads to various types of cancers, coronary and neurological ailments in human. There are several sources of arsenic exposure such as drinking water, diet, wood preservatives, smoking, air and cosmetics, while, drinking water is the most explored route. Inorganic arsenic exhibits higher levels of toxicity compared its organic forms. Exposure to inorganic arsenic is known to cause major neurological effects such as cytotoxicity, chromosomal aberration, damage to cellular DNA and genotoxicity. On the other hand, long-term exposure to arsenic may cause neurobehavioral effects in the juvenile stage, which may have detrimental effects in the later stages of life. Thus, it is important to understand the toxicology and underlying molecular mechanism of arsenic which will help to mitigate its detrimental effects. The present review focuses on the epidemiology, and the toxic mechanisms responsible for arsenic induced neurobehavioral diseases, including strategies for its management from water, community and household premises. The review also provides a critical analysis of epigenetic and transgenerational modifications, mitochondrial oxidative stress, molecular mechanisms of arsenic-induced oxidative stress, and neuronal dysfunction.

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“…As part of the cellular stress response, iAs 3+ was found to induce the expression of chaperone proteins, especially heat shock proteins HSP70 and sHSPs. − Additionally, chronic arsenite exposure was shown to up-regulate heat shock proteins via activation of DAF-16/FOXO transcription factor through oxidative stress …”

Section: Arsenic-induced Disruption Of Proteostasis Networkmentioning

confidence: 99%

Arsenic Exposure and Compromised Protein Quality Control

Tam

Wang

2020

Chem. Res. Toxicol.

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Exposure to arsenic in contaminated drinking water is a worldwide public health problem that affects more than 200 million people. Protein quality control constitutes an evolutionarily conserved mechanism for promoting proper folding of proteins, refolding of misfolded proteins, and removal of aggregated proteins, thereby maintaining homeostasis of the proteome (i.e., proteostasis). Accumulating lines of evidence from epidemiological and laboratory studies revealed that chronic exposure to inorganic arsenic species can elicit proteinopathies that contribute to neurodegenerative disorders, cancer, and type II diabetes. Here, we review the effects of arsenic exposure on perturbing various elements of the proteostasis network, including mitochondrial homeostasis, molecular chaperones, inflammatory response, ubiquitin-proteasome system, autophagy, as well as asymmetric segregation and axonal transport of misfolded proteins. We also discuss arsenic-induced disruptions of post-translational modifications of proteins, for example, ubiquitination, and their implications in proteostasis. Together, studies in the past few decades support that disruption of protein quality control may constitute an important mechanism underlying the arsenic-induced toxicity.

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Arsenic Trioxide Exposure Induces Heat Shock Protein Responses in Cock Livers

Cited by 5 publications

References 38 publications

Maternal heat stress regulates the early fat deposition partly through modification of m6A RNA methylation in neonatal piglets

Maternal heat stress regulates the early fat deposition partly through modification of m6A RNA methylation in neonatal piglets

Molecular Mechanism of Arsenic-Induced Neurotoxicity including Neuronal Dysfunctions

Arsenic Exposure and Compromised Protein Quality Control

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