IMBALANCE OF ANTIOXIDANT-PROOXIDANT SYSTEM IN RAT'S JAW BONE TISSUE UNDER LONG-TERM INTRODUCTION OF ETHANOL

Introduction. Nowadays, it is unclear what the trigger for bone resorption under the influence of chronic alcohol consumption is. As the reactions of conversion of ethanol into acetic acid are accompanied by an increase in the production of reactive oxygen species, it can be assumed that the formation of oxidative stress with prolonged alcohol consumption occurs in bone tissue as well. Aim. Research of the effect of chronic administration of ethanol to females and males laboratory rats on indices of resorption, osteogenesis, the condition of the antioxidant-prooxidant system in bone tissue. Materials and Methods. 2-month old animals received from 5 % to 15 % of ethanol in their drinking water with gradual increase of the concentration. The lower jaws were segregated, and the degree of atrophy of the alveolar process was calculated. The activity of elastase, acidic (AcF) and alkaline phosphatase (AlF), superoxide dismutase (SOD), catalase, glutathione reductase and malonic dialdehyde (MDA) content were determined in the bone tissue homogenates. Results. Chronic alcohol consumption contributed to an increase in alveolar bone atrophy, increased activity of biochemical markers of bone resorption (elastase by 32.2 %, AcF – by 33.6 %), decreased osteogenesis (AlF activity by 32.4 %). Alcohol intoxication led to oxidative imbalance of bone tissue: a decrease in SOD activity by an average of 16.9 %, glutathione reductase activity by 36.2 %, increase in catalase activity by 35.9 % and an increase in MDA levels by 51.8 %. Conclusion. Chronic alcohol consumption stimulates atrophy of the alveolar process of the rat jaw, induces oxidative imbalance in bone tissue, which can be a trigger pathogenetic factor in further development of resorption pro-inflammatory processes in bone tissue and inhibition of bone formation.

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The Loss of α- and β-Tubulin Proteins Are a Pathological Hallmark of Chronic Alcohol Consumption and Natural Brain Ageing

Brain Sciences ◽

10.3390/brainsci8090175 ◽

2018 ◽

Vol 8 (9) ◽

pp. 175 ◽

Cited By ~ 3

Author(s):

Wajana Labisso ◽

Ana-Caroline Raulin ◽

Lucky Nwidu ◽

Artur Kocon ◽

Declan Wayne ◽

...

Keyword(s):

Alcohol Consumption ◽

Protein Expression ◽

Neuronal Damage ◽

Alcohol Intoxication ◽

Post Mortem ◽

Chronic Alcohol ◽

Chronic Alcohol Consumption ◽

Protein Levels ◽

Brain Ageing ◽

Tubulin Protein

Repetitive excessive alcohol intoxication leads to neuronal damage and brain shrinkage. We examined cytoskeletal protein expression in human post-mortem tissue from Brodmann’s area 9 of the prefrontal cortex (PFC). Brain samples from 44 individuals were divided into equal groups of 11 control, 11 alcoholic, 11 non-alcoholic suicides, and 11 suicide alcoholics matched for age, sex, and post-mortem delay. Tissue from alcoholic cohorts displayed significantly reduced expression of α- and β-tubulins, and increased levels of acetylated α-tubulin. Protein levels of histone deacetylase-6 (HDAC6), and the microtubule-associated proteins MAP-2 and MAP-tau were reduced in alcoholic cohorts, although for MAPs this was not significant. Tubulin gene expressions increased in alcoholic cohorts but not significantly. Brains from rats administered alcohol for 4 weeks also displayed significantly reduced tubulin protein levels and increased α-tubulin acetylation. PFC tissue from control subjects had reduced tubulin protein expression that was most notable from the sixth to the eighth decade of life. Collectively, loss of neuronal tubulin proteins are a hallmark of both chronic alcohol consumption and natural brain ageing. The reduction of cytosolic tubulin proteins could contribute to the brain volumetric losses reported for alcoholic patients and the elderly.

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