Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An urgent need for toxicological studies on aluminium oxide nanoparticles (Al(2) [Formula: see text]NPs) has arisen from their rapidly emerging range of applications in the food and agricultural sectors. Despite the widespread use of nanoscale aluminium and its composites in the food industry, there is a serious lack of information concerning the biological activities of Al(2) [Formula: see text]NPs (ANPs) and their impact on human health. In this preliminary study, the effects of ANPs on metabolic stress in human mesenchymal stem cells (hMSCs) were analysed. The results showed dose-dependent effects, including cellular toxicity. The mitochondrial membrane potential in the hMSCs decreased with increasing ANP concentrations after 24 h of exposure. The expression levels of oxidative stress-responsive enzymes were monitored by RT-PCR. The expression levels of CYP1A and POR were up-regulated in response to ANPs, and a significant down-regulation in the expression of the antioxidant enzyme SOD was observed. Further, dose-dependent changes in the mRNA levels of GSTM3, GPX and GSR were noted. These findings suggest that the toxicity of ANPs in hMSCs may be mediated through an increase in oxidative stress. The results of this study clearly demonstrate the nanotoxicological effects of ANPs on hMSCs, which will be useful for nanotoxicological indexing.
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PMID:Aluminium oxide nanoparticles induce mitochondrial-mediated oxidative stress and alter the expression of antioxidant enzymes in human mesenchymal stem cells. 2304 73

Arable land contamination with nickel (Ni) has become a major threat to worldwide crop production. Recently, melatonin has appeared as a promising stress-relief substance that can alleviate heavy metal-induced phytotoxicity in plants. However, the plausible underlying mechanism of melatonin function under Ni stress has not been fully substantiated in plants. Herein, we conducted an experiment that unveiled critical mechanisms in favor of melatonin-mediated Ni-stress tolerance in tomato. Ni stress markedly inhibited growth and biomass by impairing the photosynthesis, photosystem function, mineral homeostasis, root activity, and osmotic balance. In contrast, melatonin application notably reinforced the plant growth traits, increased photosynthesis efficiency in terms of chlorophyll content, upregulation of chlorophyll synthesis genes, i.e. POR, CAO, CHL G, gas exchange parameters, and PSII maximum efficiency (Fv/Fm), decreased Ni accumulation and increased mineral nutrient homeostasis. Moreover, melatonin efficiently restricted the hydrogen peroxide (H2O2) and superoxide radical production and increased RBOH expression and restored cellular integrity (less malondialdehyde and electrolyte leakage) through triggering the antioxidant enzyme activities and modulating AsA-GSH pools. Notably, oxidative stress was effectively mitigated by upregulation of several defense genes (SOD, CAT, APX, GR, GST, MDHAR, DHAR) and melatonin biosynthesis-related genes (TDC, T5S, SNAT, ASMT). Besides, melatonin treatment enhanced secondary metabolites (phenols, flavonoids, and anthocyanin) contents along with their encoding genes (PAL, CHS) expression, and these metabolites potentially restricted excess H2O2 accumulation. In conclusion, our findings deciphered the potential functions of melatonin in alleviating Ni-induced phytotoxicity in tomato through boosting the biomass production, photosynthesis, nutrient uptake, redox balance, and secondary metabolism.
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PMID:Melatonin alleviates nickel phytotoxicity by improving photosynthesis, secondary metabolism and oxidative stress tolerance in tomato seedlings. 3229 96