Effect of Ethanol Administration on Activities of Some Lysosomal Hydrolases in the Mouse

Witek, B.; Kolataj, A.

doi:10.1016/s0306-3623(98)00109-8

Cited by 13 publications

(14 citation statements)

References 14 publications

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“…31 Experimental studies on animal models have also indicated that ethanol enhanced the fatty acid oxidation by kidney microsomes and peroxisomes and affected the activities of some kidney lysosomal hydrolases. 32 It is widely accepted that alcohol consumption causes disruption in the structure and function of the kidneys. White et al 33 demonstrated that, in Australian adults, self-categorization as a moderate or heavy drinker or an average consumption of 30 g of ethanol per day or more was associated with significantly elevated risks of developing albuminuria over 5 years of follow-up, compared with light alcohol consumption.…”

Section: Discussionmentioning

confidence: 99%

Melatonin and Vitamin C Ameliorate Alcohol-Induced Oxidative Stress and eNOS Expression in Rat Kidney

et al. 2012

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Objectives: The aim of this study was to investigate the preventive effects of melatonin and vitamin C as antioxidants on renal injury in chronic alcohol consumption. Materials and methods: A total of 24 adult male Wistar rats weighing 200-250 g were used in the study. Rats were divided into four equal groups. Group I (control): rats were not fed on alcohol; Group II: rats were fed on alcohol; Group III: rats were fed on alcohol and 40 mg/kg vitamin C; and Group IV: rats were fed on alcohol and 4 mg/kg melatonin. Results: Light microscopic examination revealed atrophic renal corpuscles, dilatation and congestion of the peritubular vessels, and renal corpuscles with obscure Bowman's space and a few foamy-appearing tubules due to alcohol consumption were observed. Expression of endothelial nitric oxide synthase (eNOS) was localized to glomerulus, distal, and collector tubules. eNOS staining decreased in alcohol treatment group and melatonin and vitamin C encore increased expression pattern of eNOS. Alcohol consumption increased malondialdehyde (MDA) level and superoxide dismutase (SOD) and catalase (CAT) activities significantly in the alcohol consumption groups compared with that in the control group, while in melatonin give group just MDA level was decreased statistically significant and SOD and CAT activities were also decreased numerically compared with the alcohol consumption groups. Conclusions: These results indicated that chronic alcohol consumption caused renal damage by increased lipid peroxidation and melatonin and vitamin C administration produced in some degree protection against alcohol-induced damage.

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Section: Discussionmentioning

confidence: 99%

Melatonin and Vitamin C Ameliorate Alcohol-Induced Oxidative Stress and eNOS Expression in Rat Kidney

et al. 2012

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“…For example, in liver cells of CR acyl‐ghrelin deficient ( Goat −/− ) mice, there is a reduction in the autophagosome protein LC3‐II, demonstrating a decreased rate of autophagy . The activity of various lysosomal enzymes, which are required for the breakdown of autophagosomes, is raised in the blood plasma of rabbits treated with acyl‐ghrelin . Also, acyl‐ghrelin activates autophagy in carcinoma cells .…”

Section: Calorie Restriction Regulates Brain Functionmentioning

confidence: 99%

Less is more: Caloric regulation of neurogenesis and adult brain function

Morgan

Andrews

Davies

2017

J Neuroendocrinology

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Calorie intake is essential for regulating normal physiological processes and is fundamental to maintaining life. Indeed, both extremes of calorie intake result in increased morbidity and mortality. In this review, we discuss the effect of calorie intake on adult brain function, with an emphasis on the beneficial effects of mild calorie restriction.Recent findings relating to the regenerative and protective effects of the gastrointestinal hormone, ghrelin, suggest that it may underlie the beneficial effects of calorie restriction. We discuss the putative cellular mechanisms underlying the action of ghrelin and their possible role in supporting healthy brain ageing. K E Y W O R D Sacyl-ghrelin, adult hippocampal neurogenesis, calorie restriction, diet-induced obesity | INTRODUCTIONThe energy status of an organism is tightly controlled around a setpoint by hormonal and neural systems. These neuroendocrine checks and balances promote homeostasis, thereby ensuring an appropriate energy supply for the energetic demands of metabolism, physical activity, growth and repair.Disturbances to this homeostasis result in multiple physiological impairments, including age-related conditions such as type 2 dibetes mellitus and obesity. Perhaps less well recognised are the consequences of metabolic dysfunction on neuronal health and cognition.Diet-induced obesity (DIO) is a risk factor for neurodegenerative diseases such as Parkinson's disease (PD) and dementia. Conversely, calorie restriction (CR) (ie, an approximate 30% reduction in calorie intake) protects against neurodegeneration and promotes cognitive function (Figure 1). Indeed, there is a growing body of work supporting the CR paradigm as a tool for promoting lifespan and, perhaps more importantly, healthspan.1 However, the physiological mechanisms underlying these effects are not fully understood. Here, we review literature that identifies calorie intake as an important regulator of nerve cell function, with important implications for neurodegenerative disorders. Moreover, we describe recent research showing that CR promotes new neurone formation (neurogenesis) and neuroprotection in the adult brain and discuss the possible mechanisms that underpin this effect. | CALORIE RESTRICTION REGULATES BRAIN FUNCTIONCalorie restriction, in the absence of malnutrition, has beneficial effects on brain function, including reducing the incidence of age-related neurodegenerative disease, 2 eliciting anti-depressant behaviour 3 and improving memory function in rodents. 4 In nonhuman primates, prolonged CR in adulthood decreases the incidence of age-related disease, including measures of brain atrophy and glucose regulation. 5-7Translation of the carefully controlled CR experiments from preclinical models to humans is problematic. In particular, it is difficult to re-capitulate experimental controls such as genetic background and home environment (diet, temperature and lighting) that are standard in biomedical laboratory research. Nonetheless, in adult humans, a 3-month period of CR impr...

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“…It is known that alcohol impairs the function of almost all enzymatic cell systems [47,48]. Lysosomal enzymes are involved in the catabolism of glycolipids, glycoproteins, and proteoglycans [19,49].…”

Section: Catabolism Of Glycoconjugatesmentioning

confidence: 99%

“…During ethanol intoxication, the cellular and lysosomal membranes are impaired (Table 1), and proteases, together with glycosidases, may be translocated into the cytosol fraction, the intercellular space, and the body fluids, contributing to glycoconjugate catabolism [49,51,57,58]. Acetaldehyde and reactive oxygen species, generated during alcohol intoxication, may modify proteins and lipids in the lysosomal and cellular membranes, increasing membrane fragility, thus releasing hydrolases to the cytosol and extracellular space (Figures 2, 3) [48,51,58]. The ethanol-induced displacement of membrane-bound water ( Figure 6) and decrease in ATP synthesis during alcohol consumption may also participate in destabilization of cellular membranes [24,58].…”

Section: Catabolism Of Glycoconjugatesmentioning

confidence: 99%

Alcohol abuse and glycoconjugate metabolism

Waszkiewicz

Szajda

Zalewska

et al. 2012

Folia Histochem Cytobiol.

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Abstract:The relationship between alcohol consumption and glycoconjugate metabolism is complex and multidimensional. This review summarizes the advances in basic and clinical research on the molecular and cellular events involved in the metabolic effects of alcohol on glycoconjugates (glycoproteins, glycolipids, and proteoglycans). We summarize the action of ethanol, acetaldehyde, reactive oxygen species (ROS), nonoxidative metabolite of alcohol -fatty acid ethyl esters (FAEEs), and the ethanol-water competition mechanism, on glycoconjugate biosynthesis, modification, transport and secretion, as well as on elimination and catabolism processes. As the majority of changes in the cellular metabolism of glycoconjugates are generally ascribed to alterations in synthesis, transport, glycosylation and secretion, the degradation and elimination processes, of which the former occurs also in extracellular matrix, seem to be underappreciated. The pathomechanisms are additionally complicated by the fact that the effect of alcohol intoxication on the glycoconjugate metabolism depends not only on the duration of ethanol exposure, but also demonstrates dose-and regional-sensitivity. Further research is needed to bridge the gap in transdisciplinary research and enhance our understanding of alcohol-and glycoconjugate-related diseases.

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Effect of Ethanol Administration on Activities of Some Lysosomal Hydrolases in the Mouse

Cited by 13 publications

References 14 publications

Melatonin and Vitamin C Ameliorate Alcohol-Induced Oxidative Stress and eNOS Expression in Rat Kidney

Melatonin and Vitamin C Ameliorate Alcohol-Induced Oxidative Stress and eNOS Expression in Rat Kidney

Less is more: Caloric regulation of neurogenesis and adult brain function

Alcohol abuse and glycoconjugate metabolism

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