Marisa G Repetto

Publications (7)14.98 Total impact

• Article: The protective effect of menhaden oil in the oxidative damage and renal necrosis due to dietary choline deficiency.

  Georgina P Ossani, Marisa G Repetto, Alberto Boveris, Alberto J Monserrat
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  ABSTRACT: Weanling rats fed a choline-deficient diet develop kidney oxidative damage, tubular and cortical kidney necrosis, renal failure and animal death. The effect of dietary menhaden oil was assayed on the mentioned sequence correlating oxidative stress with renal structure and function. Rats were fed ad libitum 4 different diets: (a) a choline-deficient diet with corn oil and sunflower hydrogenated oil as a source of fatty acids; (b) the same diet supplemented with choline; (c) a choline-deficient diet with menhaden oil as a source of fatty acids; and (d) the previous diet supplemented with choline. Animals were sacrificed at days 0, 2, 4 and 7. The histopathological study of the kidneys showed that renal necrosis was only observed at day 7 in choline-deficient rats receiving the vegetable oil diet, simultaneously with increased creatinine plasma levels. Homogenate chemiluminescence (BOOH-initiated chemiluminescence) and phospholipid oxidation indicate the development of oxidative stress and damage in choline-deficient rats fed vegetable oils as well as the protective effect of menhaden oil. Rats fed with the fish oil diet showed that oxidative stress and damage develop later, as compared with vegetable oil, with no morphological damage during the experimental period.
  Food & function. 12/2012;
• Article: Type 2 diabetes and/or its treatment leads to less cognitive impairment in Alzheimer's disease patients.

  Raúl O Domínguez, Enrique R Marschoff, Silvia E González, Marisa G Repetto, Jorge A Serra
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  ABSTRACT: To evaluate the cognitive performance of a homogeneous population of Alzheimer's disease (AD), non-demented Type 2 Diabetes Mellitus (DIAB), demented with concomitant diseases (AD+DIAB) and healthy control subjects. AD is a progressive dementia disorder characterized clinically by impairment of memory, cognition and behavior. Recently, a major research interest in AD has been placed on early evaluation. Diabetes is one of the clinical conditions that represent the greatest risk of developing oxidative stress and dementia. Glucose overload, leading to the development of impaired-induced insulin secretion in DIAB and has been suggested to slow or deter AD pathogenesis. The degree of cognitive impairment was determined on the Alzheimer Disease Assessment Scale-Cognitive (ADAS-Cog) and the Folstein's Mini Mental State Examination (MMSE); the severity of dementia was quantified applying the Clinical Dementia Rating (CDR) test; the Hamilton test was employed to evaluate depressive conditions; the final population studied was 101 subjects. The cognitive deterioration is statistically significantly lower (p<0.05) in AD+DIAB patients as compared with AD patients. In this longitudinal study the superimposed diabetic condition was associated with a lower rate of cognitive decline, while diabetic non-demented patients and controls present normal scores.
  Diabetes research and clinical practice 06/2012; 98(1):68-74. · 2.16 Impact Factor
• Source

  Available from: Jorge Serra

  Chapter: Free Radicals, Oxidative Stress and Oxidative Damage in Parkinson's Disease

  Marisa G. Repetto, Ra�l O. Dom�nguez, Enrique R. Marschoff, Jorge A. Serra
  02/2012; , ISBN: 978-953-307-876-2
• Article: Effects of rotenone and pyridaben on complex I electron transfer and on mitochondrial nitric oxide synthase functional activity.

  Ana Navarro, Manuel J Bández, Carmen Gómez, Marisa G Repetto, Alberto Boveris
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  ABSTRACT: Rotenone and pyridaben were tested on activities and properties of rat brain mitochondria determining Ki (inhibitor concentration at half maximal inhibition) and Imax (% of inhibition at maximal inhibitor concentration). The assayed activities were complexes I, II and IV, respiration in states 3, 3u (uncoupled) and 4, biochemical and functional activities of mitochondrial nitric oxide synthase (mtNOS), and inner membrane potential. Selective inhibitions of complex I activity, mitochondrial respiration and membrane potential with malate-glutamate as substrate were observed, with a Ki of 0.28-0.36 nmol inhibitor/mg of mitochondrial protein. Functional mtNOS activity was half-inhibited at 0.70-0.74 nmol inhibitor/mg protein in state 3 mitochondria and at 2.52-2.98 nmol inhibitor/mg protein in state 3u mitochondria. This fact is interpreted as an indication of mtNOS being structurally adjacent to complex I with an intermolecular mtNOS-complex I hydrophobic bonding that is stronger at high Δψ and weaker at low Δψ.
  Journal of Bioenergetics 10/2010; 42(5):405-12. · 2.81 Impact Factor
• Article: Oxidative damage: the biochemical mechanism of cellular injury and necrosis in choline deficiency.

  Marisa G Repetto, Georgina Ossani, Alberto J Monserrat, Alberto Boveris
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  ABSTRACT: Oxidative stress and damage are characterized by decreased tissue antioxidant levels, consumption of tissue alpha-tocopherol, and increased lipid peroxidation. These processes occur earlier than necrosis in the liver, heart, kidney, and brain of weanling rats fed a choline deficient (CD) diet. In tissues, water-soluble antioxidants were analyzed as total reactive antioxidant potential (TRAP), alpha-tocopherol content was estimated from homogenate chemiluminescence (homogenate-CL), and lipid peroxidation was evaluated by thiobarbituric acid reactive substances (TBARS). Histopathology showed hepatic steatosis at days 1-7, tubular and glomerular necrosis in kidney at days 6 and 7, and inflammation and necrosis in heart at days 6 and 7. TRAP levels decreased by 18%, 48%, 56%, and 66% at day 7, with t(1/2) (times for half maximal change) of 2.0, 1.8, 2.5, and 3.0 days in liver, kidney, heart, and brain, respectively. Homogenate-CL increased by 97%, 113%, 18%, and 297% at day 7, with t(1/2) of 2.5, 2.6, 2.8, and 3.2 days in the four organs, respectively. TBARS contents increased by 98%, 157%, 104%, and 347% at day 7, with t(1/2) of 2.6, 2.8, 3.0, and 5.0 days in the four organs, respectively. Plasma showed a 33% decrease in TRAP and a 5-fold increase in TBARS at day 5. Oxidative stress and damage are processes occurring earlier than necrosis in the kidney and heart. In case of steatosis prior to antioxidant consumption and increased lipid peroxidation, no necrosis is observed in the liver.
  Experimental and Molecular Pathology 11/2009; 88(1):143-9. · 2.42 Impact Factor
• Article: Raúl O. Domínguez; Enrique R. Marschoff; Eduardo M. Guareschi; Arturo L. Famulari; Marisa G. Repetto; Miguel A. Pagano and Jorge A. Serra. Insulin, glucose and glycated hemoglobin in Alzheimer's and vascular dementia with and without superimposed Type II diabetes mellitus condition. Journal of Neural Transmission (General Section), Springer-Verlag, Viena, Austria, v. 115, n. 1, p. 77-84, 2008.

  Enrique R. Marschoff, Eduardo M. Guareschi, Arturo L. Famulari, Marisa G. Repetto
  Journal of Neural Transmission (General Section). 09/2008;
• Article: Evidence of oxidative stress in familial amyloidotic polyneuropathy type 1.

  Mónica L Fiszman, Marianna Di Egidio, Karina C Ricart, Marisa G Repetto, Laura N Borodinsky, Susana F Llesuy, Roberto D Saizar, Pedro L Trigo, Symon Riedstra, Paulo P Costa, Andrés M Villa, Nestor Katz, Javier C Lendoire, Roberto E P Sica
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  ABSTRACT: To evaluate the oxidative state in patients with familial amyloidotic polyneuropathy type 1 (FAP1). From 3 unrelated families, patients with FAP1 carrying a transthyretin Met-30 mutation were studied. The diagnosis was confirmed by genetic analysis. Eleven of 21 patients carried the mutation; all were symptomatic and were clinically assessed using a clinical score. All of the patients were evaluated for copper-zinc superoxide dismutase type 1 activity in red blood cells using spectrophotometry. Plasma total reactive antioxidant potential was studied using a chemiluminescent method. The results were compared with those obtained from an age-matched control group. A public and academic multidisciplinary research clinic. Six of the 11 FAP1-positive patients disclosed superoxide dismutase type 1 activity values greater than 55 U/mg of protein (upper control limit), whereas 9 of 10 patients in whom total reactive antioxidant potential was measured had values below the lower limit of the control group. No relationship was found between the levels of superoxide dismutase type 1 activity and the severity of the clinical involvement. Oxidative stress may be part of the mechanisms leading to tissue damage in patients with FAP1. The lack of correlation between the laboratory findings and the severity of clinical involvement may signal that oxidative processes are at work throughout the natural history of the disease.
  Archives of Neurology 05/2003; 60(4):593-7. · 7.58 Impact Factor