Changes of DNA Damage Effect of T-2 or Deoxynivalenol Toxins during Three Weeks Exposure in Common Carp (Cyprinus carpio L.) Revealed by LORD-Q PCR

Szabó, Rubina Tünde; Kovács-Weber, Mária; Balogh, Krisztián; Mézes, Miklós; Kovács, Balázs

doi:10.3390/toxins13080576

Cited by 4 publications

(1 citation statement)

References 42 publications

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“…Therefore, research on DNA damage and its detection methods is of paramount importance. Presently, the commonly used methods for detecting DNA damage include polymerase chain reaction (PCR) ( 62 ), comet assay ( 63 ) and γ-H2AX detection ( 64 ).…”

Section: Dna Damage and Repair Mechanismsmentioning

confidence: 99%

Research progress on the role and mechanism of DNA damage repair in germ cell development

Wang

Chen

et al. 2023

Front. Endocrinol.

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In the complex and dynamic processes of replication, transcription, and translation of DNA molecules, a large number of replication errors or damage can occur which lead to obstacles in the development process of germ cells and result in a decreased reproductive rate. DNA damage repair has attracted widespread attention due to its important role in the maintenance and regulation of germ cells. This study reports on a systematic review of the role and mechanism of DNA damage repair in germline development. First, the causes, detection methods, and repair methods of DNA damage, and the mechanism of DNA damage repair are summarized. Second, a summary of the causes of abnormal DNA damage repair in germ cells is introduced along with common examples, and the relevant effects of germ cell damage. Third, we introduce the application of drugs related to DNA damage repair in the treatment of reproductive diseases and related surgical treatment of abnormal DNA damage, and summarize various applications of DNA damage repair in germ cells. Finally, a summary and discussion is given of the current deficiencies in DNA damage repair during germ cell development and future research development. The purpose of this paper is to provide researchers engaged in relevant fields with a further systematic understanding of the relevant applications of DNA damage repair in germ cells and to gain inspiration from it to provide new research ideas for related fields.

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Section: Dna Damage and Repair Mechanismsmentioning

confidence: 99%

Research progress on the role and mechanism of DNA damage repair in germ cell development

Wang

Chen

et al. 2023

Front. Endocrinol.

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Individual cytotoxicity of three major type A trichothecene, T-2, HT-2, and diacetoxyscirpenol in human Jurkat T cells

Wattanasuntorn,

Phuektes,

Poapolathep

et al. 2024

Toxicon

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Sodium butyrate alleviates T‐2 toxin–induced liver toxicity and renal toxicity in quails by modulating oxidative stress–related Nrf2 signaling pathway, inflammation, and CYP450 enzyme system

He,

Zhu,

Song

et al. 2024

Journal of Food Science

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T‐2 toxin is a member of class A aspergilloides toxins, one of the most prevalent mycotoxins that contaminate feed and food. Direct ingestion of animals or feed contaminated by T‐2 toxin can cause various animal diseases. Butyrate is an organic fatty acid featuring a four‐carbon chain, which is commonly found in the form of sodium butyrate (NaB). NaB has several biological functions and pharmacological effects. However, the role of sodium butyrate in alleviating T‐2 toxin–induced hepatorenal toxicity has not been explored. In this study, 240 juvenile quails were evenly assigned into 4 groups. The experimental setup comprised four groups: The control group received a standard diet; the toxin group received a diet containing 0.9 mg/kg T‐2 toxin; the butyrate group received a diet containing 0.5 g/kg NaB; and the T‐2 treatment group received a diet containing both 0.9 mg/kg T‐2 toxin and 0.5 g/kg NaB. We evaluated the histopathological changes in the kidney and liver on Days 14 and 28 and explored the molecular mechanisms involving oxidative stress, inflammation, and expression of nuclear xenobiotic receptors (NXRs). Our results showed that T‐2 toxin exposure–induced inflammation in the liver and kidney by activating the oxidative stress pathway and modulating expression of NXRs to regulate related CYP450 isoforms, ultimately leading to histopathological injury in the liver and kidney, whereas sodium butyrate ameliorated this injury. These results offer novel insights into the molecular mechanisms underlying the protective effects of sodium butyrate in mitigating T‐2 toxin–induced hepatorenal injury in juvenile quails.Practical ApplicationThe mechanisms of T‐2 toxin toxicity have been well described in experimental animals, but studies in birds are limited. With the development of society, the market scale of quails farming has been expanding, and the value of quails meat and eggs is increasing; there is an urgent need to clarify the harm of T‐2 toxin to quails and its mechanism.

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Changes of DNA Damage Effect of T-2 or Deoxynivalenol Toxins during Three Weeks Exposure in Common Carp (Cyprinus carpio L.) Revealed by LORD-Q PCR

Cited by 4 publications

References 42 publications

Research progress on the role and mechanism of DNA damage repair in germ cell development

Research progress on the role and mechanism of DNA damage repair in germ cell development

Individual cytotoxicity of three major type A trichothecene, T-2, HT-2, and diacetoxyscirpenol in human Jurkat T cells

Sodium butyrate alleviates T‐2 toxin–induced liver toxicity and renal toxicity in quails by modulating oxidative stress–related Nrf2 signaling pathway, inflammation, and CYP450 enzyme system

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