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Pesticide treatment leads to a significant increase in wheat yield and enhances pest resistance. However, pesticides, particularly the insecticide cypermethrin, which is used for wheat Triticum aestivum L. field and grain storage treatment, are toxic xenobiotics. To reduce their toxicity, it is possible to pre-treat seeds with plant growth-promoting rhizobacteria (PGPR), which can enhance plant resistance to adverse environmental factors. In this study, we used a previously unused as PGPR representative of the genus Azospirillum, A. thiophilum BV-ST, isolated in Russia, which makes it interesting for agricultural use in the same climatic zone. We optimized the detection method of A. thiophilum using PCR. Then, we demonstrated that this bacterium successfully inoculates to wheat roots. We showed that cypermethrin treatment of one- and two-week-old wheat seedlings caused an increase in mtDNA damage, and in one-week-old seedlings, it induced a decrease in chlorophyll levels. However, three- and four-week-old seedlings were more resistant to damage, possibly due to their approximately 5-fold higher expression of NDOR-1 and GST genes, which play an important role in xenobiotic detoxification. Pre-treatment of wheat seeds with A. thiophilum contributed to the upregulation of NDOR-1 and GST gene expression in one- and two-week-old seedlings, resulting in the protection of mtDNA from cypermethrin-induced damage and prevented the decrease in chlorophyll levels. [ABSTRACT FROM AUTHOR]

Reduced cellular response to insulin in skeletal muscle is one of the major components of the development of type 2 diabetes (T2D). Mitochondrial dysfunction involves in the accumulation of toxic reactive oxygen species (ROS) that leads to insulin resistance. The aim of this study was to verify the involvement of mitochondrial DNA damage at ROS generation in skeletal muscle during development of T2D. Wistar rats were fed a diet containing 60% fat over 8 weeks and at day 14 a single injection of STZ (25 mg/kg) was administered (T2D-induced). Control rats received standard food and an injection of citrate buffer. Blood and soleus muscle were collected. Abdominal fat was quantified as well as glucose, triglyceride, LDL, HDL, and total cholesterol in plasma and mtDNA copy number, cytochrome b (cytb) mRNA, 8-hydroxyguanosine, and 8-isoprostane (a marker of ROS) in soleus muscle. T2D-induced animal presented similar characteristics to humans that develop T2D such as changes in blood glucose, abdominal fat, LDL, HDL and cholesterol total. In soleus muscle 8-isoprostane, mtDNA copy number and 8-hydroxyguanosine were increased, while cytb mRNA was decreased in T2D. Our results suggest that in the development of T2D, when risks factors of T2D are present, intracellular oxidative stress increases in skeletal muscle and is associated with a decrease in cytb transcription. To overcome this process mtDNA increased but due to the proximity of ROS generation, mtDNA remains damaged by oxidation leading to an increase in ROS in a vicious cycle accounting to the development of insulin resistance and further T2D. [ABSTRACT FROM AUTHOR]

Anti-synthetase syndrome is an autoimmune disease characterized by autoantibodies toward amino acyl-tRNA synthetases (ARS), anti-Jo 1 being the most commonly detected. Muscle damage develops in up to 90% of ARS-positive patients, characterized by a necrotizing myositis restricted to the perifascicular region. This topographic distribution of muscle damage may lead to a misdiagnosis of dermatomyositis (DM) at muscle biopsy. We compared morphological, immunohistochemical, and histoenzymatic features of muscle from ARS-positive patients (n = 11) with those of DM (n = 7) providing clues for their differential diagnosis. In addition, we evaluated markers of mitochondrial damage to provide a further distinction between these two entities. Necrosis occurred in the majority of ARS patients, mainly located in the perifascicular region. It was often limited to small foci of fibers, always associated with myocyte regeneration. This last often overwhelmed necrosis, representing occasionally the main finding. In DM, necrosis/regeneration was scarce while the peculiar feature was a diffuse atrophy of perifascicular fibers. These last showed decreased cytochrome c oxidase (COX) stain and mitochondrial DNA depletion, consistent with mitochondrial dysfunction. In contrast to DM, ARS displayed scattered COX-deficient fibers, not restricted to the perifascicular region. This feature occurred in up to 91% of patients, being prominent only in two. [ABSTRACT FROM AUTHOR]

Mitochondrial dysfunction has been associated with late onset neurodegenerative disorders, among which is Machado-Joseph disease (MJD/SCA3). In a previous study, using a transgenic mouse model of MJD, we reported a decrease in mitochondrial DNA (mtDNA) copy number and an accumulation of the 3876-bp deletion with age and with phenotype development. We extended this study by analyzing the pattern of mtDNA depletion and the accumulation of the 3876-bp deletion in 12 older transgenic (TG) and 4 wild-type (wt) animals, and by investigating the accumulation of somatic mutations in the D-loop region in 76 mice (42 TG and 34 wt). mtDNA damage was studied in TG and wt mice at different ages and tissues (blood, pontine nuclei, and hippocampus). Results for older mice demonstrate an accumulation of the mtDNA 3867-bp deletion with age, which was more pronounced in TG animals. Furthermore, the tendency for mtDNA copy number decrease with age, in all analyzed tissues of TG and wt animals, was also confirmed. No point mutations were detected in the D-loop, neither in TG nor wt animals, in any of the tissues analyzed. Due to the absence of mtDNA somatic mutations, we can suggest that mtDNA point mutation accumulation cannot be used to monitor the development and progression of the phenotype in this mouse model and likely in any MJD mice model. The present results further confirm not only the association between mtDNA alterations (copy number and deletions) and age, but also between such alterations and the expression of the mutant ataxin-3 in TG mice. [ABSTRACT FROM AUTHOR]

The current study examined the effects of ochratoxin A (OTA) and methanol on mitochondrial DNA (mtDNA). The results showed that methanol application caused approximately 29 % more damage than the control group, and that there were no significant differences among the other groups in terms of mtDNA damage. The application of 0.04 ng/mL OTA and 0.04 ng/mL OTA with methanol increased mtDNA copy number compared with the control and 0.005 ng/mL OTA with methanol groups. The copy number in the 0.04 ng/mL OTA group was approximately 16 % greater than in the control. [ABSTRACT FROM AUTHOR]

This work investigates the association between longevity, mitochondrial DNA (mtDNA) variants and oxidative DNA damage in an older than 85 years population. The participants, similar in genetic and cultural background as well as gender distribution, come from villages near to the Pyrenees Mountains (900–1,400 m altitude) ( n = 69) and the Ebro’s Valley (200–300 m altitude) ( n = 69) in Spain. Our results show an accumulation of the haplogroup J in elderly individuals with an over-representation of J2 in Pyrenees group but not in the Ebro’s Valley, the former associating with a diminished DNA damage. In conclusion, our results suggest that J mitochondrial variant, that induce lower mtDNA damage, could present a phenotypic survival advantage to environmental conditions and, thus, accumulate in elderly population. [ABSTRACT FROM AUTHOR]