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Marcella Renis

Researcher at University of Catania

Publications -  98
Citations -  3101

Marcella Renis is an academic researcher from University of Catania. The author has contributed to research in topics: Oxidative stress & DNA damage. The author has an hindex of 32, co-authored 98 publications receiving 2891 citations. Previous affiliations of Marcella Renis include University of Bari & University of Camerino.

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Reduced transcription of mitochondrial DNA in the senescent rat. Tissue dependence and effect of L-carnitine.

TL;DR: The results suggest that the age-dependent impairment of both heavy-strand mitochondrial DNA transcription units is related to altered environmental conditions which acetyl-L-carnitine, a substance which acts by stimulating, directly or indirectly, the energy metabolism, is able to remove.
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Free radical scavenging capacity and protective effect of Bacopa monniera L. on DNA damage.

TL;DR: Experimental evidence suggests that because of its antioxidant activity, this Ayurvedic drug may be useful in the treatment of human pathologies in which free radical production plays a key role.
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Hydroxytyrosol lipophilic analogues: Enzymatic synthesis, radical scavenging activity and DNA oxidative damage protection

TL;DR: The olive oil phenol hydroxytyrosol and its lipophilic derivatives showed very good DPPH and homovanillic alcohol 4 and its analogues 10-14 resulted scarcely effective both as radical scavengers and antioxidant agents.
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Stress Proteins and SH-Groups in Oxidant-Induced Cellular Injury After Chronic Ethanol Administration in Rat

TL;DR: The hypothesis that HSP70 induction protects the different brain areas against oxidative stress is supported and supports the hypothesis that lipid peroxides play an important role in the pathogenesis of ethanol-induced cellular injury.
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Stress proteins and SH-groups in oxidant-induced cell damage after acute ethanol administration in rat

TL;DR: The results demonstrate that elevated doses of ethanol induce HSP in various brain areas, namely, cerebellum, hippocampus, and to a lesser extent, striatum or liver, and support the hypothesis that a redox mechanism may be involved in the heat-shock signal pathway.