Germ cells of male mice express genes for peroxisomal metabolic pathways implicated in the regulation of spermatogenesis and the protection against oxidative stress

2011 ◽  
Vol 136 (4) ◽  
pp. 413-425 ◽  
Author(s):  
Sandra Dastig ◽  
Anca Nenicu ◽  
David M. Otte ◽  
Andreas Zimmer ◽  
Jürgen Seitz ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Camille Dupuy ◽  
Pierre Castelnau ◽  
Sylvie Mavel ◽  
Antoine Lefevre ◽  
Lydie Nadal-Desbarats ◽  
...  

AbstractAttention-Deficit Hyperactivity Disorder (ADHD) is one of the most common neurodevelopmental disorder characterized by inattention, impulsivity, and hyperactivity. The neurobiological mechanisms underlying ADHD are still poorly understood, and its diagnosis remains difficult due to its heterogeneity. Metabolomics is a recent strategy for the holistic exploration of metabolism and is well suited for investigating the pathophysiology of diseases and finding molecular biomarkers. A few clinical metabolomic studies have been performed on peripheral samples from ADHD patients but are limited by their access to the brain. Here, we investigated the brain, blood, and urine metabolomes of SHR/NCrl vs WKY/NHsd rats to better understand the neurobiology and to find potential peripheral biomarkers underlying the ADHD-like phenotype of this animal model. We showed that SHR/NCrl rats can be differentiated from controls based on their brain, blood, and urine metabolomes. In the brain, SHR/NCrl rats displayed modifications in metabolic pathways related to energy metabolism and oxidative stress further supporting their importance in the pathophysiology of ADHD bringing news arguments in favor of the Neuroenergetic theory of ADHD. Besides, the peripheral metabolome of SHR/NCrl rats also shared more than half of these differences further supporting the importance of looking at multiple matrices to characterize a pathophysiological condition of an individual. This also stresses out the importance of investigating the peripheral energy and oxidative stress metabolic pathways in the search of biomarkers of ADHD.


2012 ◽  
Vol 29 (9) ◽  
pp. 991-999 ◽  
Author(s):  
Yuanxiang Jin ◽  
Xiuhong Pan ◽  
Zhengwei Fu

2015 ◽  
Vol 39 (1) ◽  
pp. 229-236 ◽  
Author(s):  
Ling Liu ◽  
Runhua Tao ◽  
Jie Huang ◽  
Xingzhi He ◽  
Lanya Qu ◽  
...  

Aging ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 8710-8727 ◽  
Author(s):  
Dejiang Pang ◽  
Chengcheng Yang ◽  
Qihui Luo ◽  
Chao Li ◽  
Wentao Liu ◽  
...  

2021 ◽  
Vol 21 (Suppliment-1) ◽  
pp. 1430-1434
Author(s):  
Tuqa Sabbar Rahi ◽  
Wifaq j. albazi ◽  
Ali K. Aljarah ◽  
Alaa Hussein AL-Safy

Author(s):  
J. Pečevski ◽  
D. Radivojević ◽  
N. Savković ◽  
Lj. Vuksanović ◽  
P. Cvetković

2022 ◽  
Vol 62 (1) ◽  
pp. 617-639
Author(s):  
Xiaojing Wang ◽  
Qirong Lu ◽  
Jingchao Guo ◽  
Irma Ares ◽  
Marta Martínez ◽  
...  

Glyphosate (GLYP) is a widely used pesticide; it is considered to be a safe herbicide for animals and humans because it targets 5-enolpyruvylshikimate-3-phosphate synthase. However, there has been increasing evidence that GLYP causes varying degrees of toxicity. Moreover, oxidative stress and metabolism are highly correlated with toxicity. This review provides a comprehensive introduction to the toxicity of GLYP and, for the first time, systematically summarizes the toxicity mechanism of GLYP from the perspective of oxidative stress, including GLYP-mediated oxidative damage, changes in antioxidant status, altered signaling pathways, and the regulation of oxidative stress by exogenous substances. In addition, the metabolism of GLYP is discussed, including metabolites,metabolic pathways, metabolic enzymes, and the toxicity of metabolites. This review provides new ideas for the toxicity mechanism of GLYP and proposes effective strategies for reducing its toxicity.


Author(s):  
Paulina Nguyen-Powanda ◽  
Bernard Robaire

Abstract The efficiency of antioxidant defense system decreases with aging, thus resulting in high levels of reactive oxygen species (ROS) and DNA damage in spermatozoa. This damage can lead to genetic disorders in the offspring. There are limited studies investigating the effects of the total loss of antioxidants, such as superoxide dismutase-1 (SOD1), in male germ cells as they progress through spermatogenesis. In this study, we evaluated the effects of aging and removing SOD1 (in male germ cells of SOD1-null (Sod1−/−) mice) in order to determine the potential mechanism(s) of DNA damage in these cells. Immunohistochemical analysis showed an increase in lipid peroxidation and DNA damage in the germ cells of aged wild-type (WT) and Sod1−/− mice of all age. Immunostaining of OGG1, a marker of base excision repair (BER), increased in aged WT and young Sod1−/− mice. In contrast, immunostaining intensity of LIGIV and RAD51, markers of non-homologous end-joining (NHEJ) and homologous recombination (HR), respectively, decreased in aged and Sod1−/− mice. Gene expression analysis showed similar results with altered mRNA expression of these key DNA repair transcripts in pachytene spermatocytes and round spermatids of aged and Sod1−/− mice. Our study indicates that DNA repair pathway markers of BER, NHEJ, and HR are differentially regulated as a function of aging and oxidative stress in spermatocytes and spermatids, and aging enhances the repair response to increased oxidative DNA damage, whereas impairments in other DNA repair mechanisms may contribute to the increase in DNA damage caused by aging and the loss of SOD1.


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