Binge and Subchronic Exposure to Ketamine Promote Memory Impairments and Damages in the Hippocampus and Peripheral Tissues in Rats: Gallic Acid Protective Effects

Brum, Gerson Fernandes de; Rosa, Higor Zuquetto; Rossato, Domênika Rubert; Rosa, Jéssica Leandra Oliveira da; Metz, Vinícia Garzella; Milanesi, Laura Hautrive; Bürger, Marilise Escobar

doi:10.1007/s12640-020-00215-y

Cited by 6 publications

(4 citation statements)

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“…[ 25 ] Besides, GA effectively diminished neuroinflammation induced by lipopolysaccharides by attenuating protein aggregation and necroptosis in rats. [ 20 ] GA reportedly protected against ketamine‐induced memory impairments and lesions in the brain of rats, [ 26 ] rescued cognitive failure in APP/PS1 double transgenic mouse via interference with Aβ(1‐42) aggregation, [ 27 ] and effectively inhibited aflatoxin production in Aspergillus flavus . [ 28 ] Recent studies from our laboratories demonstrated the ameliorative influence of GA on AFB 1 ‐mediated hepatorenal and reproductive damage in rats.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective role of gallic acid in aflatoxin B₁‐induced behavioral abnormalities in rats

Adedara

Owumi

Oyelere

et al. 2020

J Biochem & Molecular Tox

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The neurotoxic impact of dietary exposure to aflatoxin B1 (AFB1) is documented in experimental and epidemiological studies. Gallic acid (GA) is a triphenolic phytochemical with potent anticancer, anti‐inflammatory, and antioxidant activities. There is a knowledge gap on the influence of GA on AFB1‐induced neurotoxicity. This study probed the influence of GA on neurobehavioral and biochemical abnormalities in rats orally treated with AFB1 per se (75 µg/kg body weight) or administered together with GA (20 and 40 mg/kg) for 28 uninterrupted days. Behavioral endpoints obtained with video‐tracking software demonstrated significant (p < .05) abatement of AFB1‐induced anxiogenic‐like behaviors (increased freezing, urination, and fecal bolus discharge), motor and locomotor inadequacies, namely increased negative geotaxis and diminished grip strength, absolute turn angle, total time mobile, body rotation, maximum speed, and total distance traveled by GA. The improvement of exploratory behavior in animals that received both AFB1 and GA was confirmed by track plots and heat maps appraisal. Abatement of AFB1‐induced decreases in acetylcholinesterase activity, antioxidant status and glutathione level by GA was accompanied by a marked reduction in oxidative stress markers in the cerebellum and cerebrum of rats. Additionally, GA treatment abrogated AFB1‐mediated decrease in interleukin‐10 and elevation of inflammatory indices, namely tumor necrosis factor‐α, myeloperoxidase activity, interleukin‐1β, and nitric oxide. Further, GA treatment curtailed caspase‐3 activation and histological injuries in the cerebral and cerebellar tissues. In conclusion, abatement of AFB1‐induced neurobehavioral abnormalities by GA involves anti‐inflammatory, antioxidant, and antiapoptotic mechanisms in rats.

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Section: Introductionmentioning

confidence: 99%

Neuroprotective role of gallic acid in aflatoxin B₁‐induced behavioral abnormalities in rats

Adedara

Owumi

Oyelere

et al. 2020

J Biochem & Molecular Tox

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“…The balance disruption between pro-oxidant phenomena and cellular antioxidant defenses is called oxidative stress. Once the production of reactive species or pro-oxidant phenomena overlaps the body's antioxidant capacity, there will be associated oxidative damage (Brum et al, 2020;Schimites et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, a compensatory increase in the enzymatic (CAT) and nonenzymatic (GSH and VIT C) antioxidant system was observed in the infected group compared to the control one. This oxidative stress evidence may be associated with several complications that induce cell membrane damage (Brum et al, 2020;Frey et al, 2006;Lazarotto et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Eurythrematosis as a developmental model of the Diabetes Mellitus type 1 pathological condition: pathophysiological parameters and oxidative stress / Eurytrematose como modelo de desenvolvimento da patologia da Diabetes Mellitus tipo 1: parâmetros fisiopatológicos e stress oxidativo

Rosa¹,

Nodari²,

Suthovski³

et al. 2021

BJDV

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Eurytrematosis is a helminthic disease caused by trematodes belonging to the genus Eurytrema spp. that parasitize the pancreas of many animals and humans. This parasitosis causes chronic fibrosing pancreatitis, fat infiltration in the pancreatic parenchyma, besides damaging the exocrine pancreas, which is similar to that found in patients with Diabetes Mellitus type 1 (DM1). The current work aimed to evaluate the use of bovine pancreas infected with E. coelomaticum as a model to study DM1 pathophysiology. It was carried out macroscopic analyses, parasite identification, total pancreatic lipid determination and oxidative damage biomarkers levels of pancreas naturally infected with E. coelomaticum. Macroscopically, we observed that the infected pancreas had duct obstruction, organ stiffness due to the visible presence of fibrosis, increased adipose tissue deposition, increased protein and lipid damage, as well as increased antioxidant biomarkers (GSH, CAT and VIT C). Thus, it is possible to show that DM1 may have pancreatic parasitism as a possible primary origin. However, more studies are needed to better investigate this possible primary origin; the results obtained here suggest that the use of pancreas parasitized by E. coelomaticum could be a model to investigate DM1 pathophysiology.

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“…Ketamine, on the other hand, presents its use primarily linked to a medical context, as a sedative analgesic and general anesthetic, and more recently being proposed for affective disorders treatment [ 189 , 190 ]. However, ketamine has become popular as a recreational drug, used acutely or in a binge pattern; orally, inhaled, or injected; and alone or associated with alcoholic beverages or stimulants [ 191 ]. Each of these paradigms must be examined to identify potential synergistic points and risks related to this combination [ 11 , 12 , 13 ].…”

Section: Potential Pharmacological Interactions Between Ketamine and ...mentioning

confidence: 99%

Ketamine plus Alcohol: What We Know and What We Can Expect about This

Kobayashi

Farias

Luz

et al. 2022

IJMS

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Drug abuse has become a public health concern. The misuse of ketamine, a psychedelic substance, has increased worldwide. In addition, the co-abuse with alcohol is frequently identified among misusers. Considering that ketamine and alcohol share several pharmacological targets, we hypothesize that the consumption of both psychoactive substances may synergically intensify the toxicological consequences, both under the effect of drugs available in body systems and during withdrawal. The aim of this review is to examine the toxicological mechanisms related to ketamine plus ethanol co-abuse, as well the consequences on cardiorespiratory, digestive, urinary, and central nervous systems. Furthermore, we provide a comprehensive discussion about the probable sites of shared molecular mechanisms that may elicit additional hazardous effects. Finally, we highlight the gaps of knowledge in this area, which deserves further research.

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Binge and Subchronic Exposure to Ketamine Promote Memory Impairments and Damages in the Hippocampus and Peripheral Tissues in Rats: Gallic Acid Protective Effects

Cited by 6 publications

References 70 publications

Neuroprotective role of gallic acid in aflatoxin B₁‐induced behavioral abnormalities in rats

Neuroprotective role of gallic acid in aflatoxin B₁‐induced behavioral abnormalities in rats

Eurythrematosis as a developmental model of the Diabetes Mellitus type 1 pathological condition: pathophysiological parameters and oxidative stress / Eurytrematose como modelo de desenvolvimento da patologia da Diabetes Mellitus tipo 1: parâmetros fisiopatológicos e stress oxidativo

Ketamine plus Alcohol: What We Know and What We Can Expect about This

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Binge and Subchronic Exposure to Ketamine Promote Memory Impairments and Damages in the Hippocampus and Peripheral Tissues in Rats: Gallic Acid Protective Effects

Cited by 6 publications

References 70 publications

Neuroprotective role of gallic acid in aflatoxin B1‐induced behavioral abnormalities in rats

Neuroprotective role of gallic acid in aflatoxin B1‐induced behavioral abnormalities in rats

Eurythrematosis as a developmental model of the Diabetes Mellitus type 1 pathological condition: pathophysiological parameters and oxidative stress / Eurytrematose como modelo de desenvolvimento da patologia da Diabetes Mellitus tipo 1: parâmetros fisiopatológicos e stress oxidativo

Ketamine plus Alcohol: What We Know and What We Can Expect about This

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Neuroprotective role of gallic acid in aflatoxin B₁‐induced behavioral abnormalities in rats

Neuroprotective role of gallic acid in aflatoxin B₁‐induced behavioral abnormalities in rats