Adiponectin deficiency accelerates brain aging via mitochondria-associated neuroinflammation.

BACKGROUND: A wide spectrum of changes occurs in the brain with age, from molecular to morphological aspects, and inflammation accompanied by mitochondria dysfunction is one of the significant factors associated with age. Adiponectin (APN), an essential adipokine in glucose and lipid metabolism, is involved in the aging; however, its role in brain aging has not been adequately explored. Here, we aimed to explore the relationship between APN deficiency and brain aging using multiple biochemical and pharmacological methods to probe APN in humans, KO mice, primary microglia, and BV2 cells. RESULTS: We found that declining APN levels in aged human subjects correlated with dysregulated cytokine levels, while APN KO mice exhibited accelerated aging accompanied by learning and memory deficits, anxiety-like behaviors, neuroinflammation, and immunosenescence. APN-deficient mice displayed aggravated mitochondrial dysfunction and HDAC1 upregulation. In BV2 cells, the APN receptor agonist AdipoRon alleviated the mitochondrial deficits and aging markers induced by rotenone or antimycin A. HDAC1 antagonism by Compound 60 (Cpd 60) improved mitochondrial dysfunction and age-related inflammation, as validated in D-galactose-treated APN KO mice. CONCLUSION: These findings indicate that APN is a critical regulator of brain aging by preventing neuroinflammation associated with mitochondrial impairment via HDAC1 signaling.

[Regulation of PARP-1 deficiency on epidermal growth factor receptor during lung injury of mice induced by benzo [a] pyrene inhalation exposure].

OBJECTIVE: To investigate the regulation of PARP-1 deficiency on epidermal growth factor receptor(EGFR) during lung injury of mice induced by benzo[a]pyrene(B[a]P) inhalation exposure. METHODS: PARP-1 knockout mice(PARP-1~(-/-)) and WT mice were selected as the object, and which were randomly assigned into either an intervention or a control group(n=40, half male and half female). The intervention group were individually treated with 10.0 µg/m~(3 )B[a]P for 180 days by dynamic inhalation exposure(6 h per day and 5 days per week), and the control group was given the solvent dimethyl sulfoxide(DMSO) during the same period. The expression of EGFR in lung tissues of animals were examined by RT-PCR, Western blot and immunofluorescence. RESULTS: In WT mice, the intervention manifested significant increase expression of EGFR in lung tissue, but no changes were found in the control. In PARP-1~(-/-) mice, the intervention manifested significant inhibition expression of EGFR, but the control group exhibited no changes. CONCLUSION: PARP-1 deficiency suppresses the abnormal activation of EGFR during lung injury of mice induced by B[a]P inhalation exposure.

Efficient removal of heavily oil-contaminated soil using a combination of fenton pre-oxidation with biostimulated iron and bioremediation.

Crude oil contamination severely deteriorates soils quality. Bioremediation utilizing soil indigenous organisms could be employed to decompose petroleum hydrocarbons thanks to its low cost and minor environmental disturbance. However, slow kinetics limit the successful application of this biotechnique. Pretreating oil-contaminated soils with Fenton pre-oxidation could accelerate the subsequent bioremediation process. This study was to explore the mechanisms behind the rapid propagation of indigenous petroleum-degrading bacteria (IPDB) and the efficient degradation of total petroleum hydrocarbons (TPH) in soil after Fenton pre-oxidation with biostimulated iron. Biostimulated iron and non-biostimulated iron were used in the experiments, where Fenton pre-oxidation was combined with the bioremediation of oil-contaminated soil (TPH = 13221 mg/kg). Although the amount of Fenton pre-oxidized TPH (3331-3775 mg/kg) was similar with biostimulated and non-biostimulated irons, the biodegradation of TPH after Fenton pre-oxidation with biostimulated iron (5840 mg/kg) was much higher than that with non-biostimulated iron (3034-4034 mg/kg). Moreover, abundant nutrients and a high population of residual IPDB were found after Fenton pre-oxidation with biostimulated iron, which benefited stable consumption of NH3-N and dissolved organic carbon (DOC) by IPDB during the subsequent bioremediation. However, Fenton pre-oxidation with non-biostimulated iron either resulted in greater damage to IPDB or produced fewer nutrients, thereby failing to ensure the continuous propagation of IPDB during the subsequent bioremediation. Therefore, we propose that Fenton pre-oxidation with biostimulated iron should be applied to heavily oil-contaminated soils prior to bioremediation.

Efficient cyclic oxidation of macro long-chain alkanes in soil using Fenton oxidation with recyclable Fe.

Recyclable Fe in soil was prepared by using fermented food waste supernatant. The efficient cyclic oxidation of long-chain alkanes in oil-contaminated soils could be achieved by Fenton oxidation with the recyclable Fe. The oxidation efficiency of macro long-chain alkanes (C27-C30) from the first cycle (63.4%) to the last cycle (60.1%) showed no significant decrease during three-cycle Fenton oxidation with the recyclable Fe. However, for the oil-absorbing Fe prepared by HA and Fe-SOM prepared by Cs, the oxidation efficiency of C27-C30 could not be efficiently cyclic oxidized during three-cycle Fenton oxidation. Further analysis showed that the proportion of Fe(III) in the recyclable Fe was higher than that in the oil-absorbing Fe or the Fe-SOM, where the iron content was similar. Moreover, more fulvic-like acid and humic-like acid were found in the recyclable Fe, and thus many Fe(III) ions simultaneously combined with the fulvic-like acid and humic-like acid through -C-O-C and CË­O bonds in the recyclable Fe. It was the recyclable Fe with such a stable structure that could still maintain high catalytic activity and efficiently cyclic oxidize macro long-chain alkanes during three-cycle Fenton oxidation, which is valuable for its repeated use.

The effects of di-2-ethylhexyl phthalate on testicular ultrastructure and hormone-regulated gene expression in male rats.

The objective of this study is to determine testicular pathological damage and explore its molecular mechanisms after di-2-ethylhexyl phthalate (DEHP) treatment. A total of 40 healthy 5-week-old male Sprague-Dawley rats were randomly divided into four groups, which received intragastric administration of 0 mg kg-1, 100 mg kg-1, 500 mg kg-1 and 1500 mg kg-1 DEHP for six continuous weeks. After DEHP treatment, the testes wet weight and testes coefficient were calculated, the histopathological changes of the testes were examined by HE staining and the testicular ultrastructure was examined by transmission electron microscopy. The gene expression levels were analyzed by quantitative RT-PCR and the protein expression levels were analyzed by western blotting. Both 500 mg kg-1 and 1500 mg kg-1 DEPH treatments decreased the wet weight of the testes and testes coefficient, due to vacuoles in Sertoli cells, broken mitochondrial ridges, and degranulation. Quantitative RT-PCR showed that the relative gene expression levels of steroidogenic acute regulatory protein (StAR) and 3ß-hydroxysteroid dehydrogenase (3ß-HSD) increased in the 100 mg kg-1, 500 mg kg-1, and 1500 mg kg-1 DEHP groups, respectively. Additionally, 17ß-hydroxysteroid dehydrogenase (17ß-HSD) expression levels were increased in the 1500 mg kg-1 DEHP treatment group. Gonadotropin-releasing hormone (GnRH) expression levels were decreased with 500 mg kg-1 and 1500 mg kg-1 DEHP treatments. DEHP induced serious pathological damage and ultrastructure changes in rat testes, caused endocrine disorders, interfered with the synthesis of male hormones, and ultimately led to male reproductive system dysfunction.