{"id":1709,"date":"2015-03-28T08:35:40","date_gmt":"2015-03-28T08:35:40","guid":{"rendered":"http:\/\/biomedpharmajournal.org\/?p=1709"},"modified":"2017-01-04T06:56:36","modified_gmt":"2017-01-04T06:56:36","slug":"changes-in-systemic-blood-pressure-and-serum-xanthine-oxidase-activity-induced-by-the-stimulation-of-alcohol-metabolism-by-fructose-in-man","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol4no1\/changes-in-systemic-blood-pressure-and-serum-xanthine-oxidase-activity-induced-by-the-stimulation-of-alcohol-metabolism-by-fructose-in-man\/","title":{"rendered":"Changes in Systemic Blood Pressure and Serum Xanthine Oxidase Activity Induced by The Stimulation of Alcohol Metabolism by Fructose in Man"},"content":{"rendered":"

Introduction<\/strong><\/p>\n

In addition to the oxidation of blood ethanol to acetaldehyde (ethanol + NAD+<\/sup>\u00a0\u00a0\u00a0\u00a0 acetaldehyde + NADH + H+<\/sup> ) by the cytosolic alcohol dehydrogenase, ADH, and then, to acetate (acetaldehyde + NAD+<\/sup>\u00a0\u00a0 acetate + NADH + H+<\/sup>) by\u00a0 the low Km<\/sub>\u00a0 mitochondrial acetaldehyde dehydrogenase, ALDH, the activities of these enzymes also produce excess NADH in the liver (Peters and Preedy, 1998). The generation of high amounts of NADH seems to influence a number of metabolic disorders associated with chronic alcohol consumption.\u00a0 Some of these disorders include increased reactive oxygen species (ROS) reactivities (Bailey, et al<\/em>., 1999), oxidation of endothelial nitric oxide, NO (Bailey and Cunningham, 1998), known to stimulate xanthine oxidase activity (Houston, et al<\/em>., 1998).<\/p>\n

Fructose has been reported to increase the rate of blood alcohol elimination (Onyesom and Anosike, 2004) by accepting reducing equivalents from NADH to generate NAD+<\/sup> for\u00a0 enhanced alcohol oxidation (Berman, et al<\/em>., 2003). Therefore, fructose may be able to ameliorate the associated\u00a0 metabolism disturbances and reverse the effects of alcohol in the body.<\/p>\n

In this study, the changes in serum xanthine oxidase activity and blood pressure measures induced by fructose enhanced elimination of alcohol from blood stream were assessed in order to ascertain the theoretical tendency of fructose to reduce or prevent alcohol metabolic disorders.<\/p>\n

Materials and Methods<\/strong><\/p>\n

Subjects<\/strong><\/p>\n

Twenty-two consenting male individuals in apparent good health, between the ages of 27-34 years and weighing between 56-63 kg were enlisted for the study.<\/p>\n

The volunteers were tested at two different times separated by 14 days.\u00a0 On the first occasion, they were given a single dose of 0.70g (190 proof USP) ethanol\/kg body weight after diluting to 20% with orange juice.\u00a0 On the second occasion, 0.5g fructose\/kg body weight was orally administered after about 18-23 min of ingesting the same single dose of ethanol.<\/p>\n

Blood pressure measurement<\/strong><\/p>\n

Before blood sample collection, blood pressure measurements were taken after about 10-12 min of rest in a well seated position as earlier described (Onyesom, 2002) using the full automated digital arm blood pressure monitor (SE-7000: Seinex Electronics, Ltd., UK).<\/p>\n

Blood sample collection<\/strong><\/p>\n

At different specified post administration time intervals (0, 90 and\u00a0 720 min), fasting intravenous whole blood samples were collected into sterile plain tubes, centrifuged at 1200 X g for 5 min at room temperature (27-310<\/sup>C).\u00a0 The supernatant (serum) was decanted into bijou bottle and analyzed fresh within the hour of collection.<\/p>\n

Determination of serum xanthine oxidase activity<\/strong><\/p>\n

Serum xanthine oxidase activity was assayed by the decoloration of methylene blue (Eissenthal and Danson, 1992) using spectrophotometer.<\/p>\n

Statistics<\/strong><\/p>\n

Analysis of variance (ANOVA) was used to compare mean values and P<0.05 was considered significant (Winer, et al<\/em>., 1991).<\/p>\n

Results<\/strong><\/p>\n

The results obtained are shown on Table 1. Table 1\u00a0 has the records of the mean values obtained for the changes in serum xanthine oxidase activity and blood pressure measures induced by ethanol alone and ethanol + fructose in man.<\/p>\n

Table 1: Changes in serum xanthine oxidase activity and blood pressure induced by ethanol and ethanol + fructose in man.<\/strong><\/p>\n\n\n\n\n\n\n\n
Administrations\u00a0<\/strong><\/p>\n

 <\/p>\n

 <\/td>\n

Ethanol alone<\/strong><\/p>\n

(0.7g\/kg)<\/strong><\/td>\n

Ethanol + fructose<\/strong><\/p>\n

(0.7g+0.5g\/kg)<\/strong><\/td>\n

<\/td>\n<\/tr>\n
Post administration time (h)<\/strong><\/td>\n0<\/td>\n1.5<\/td>\n15<\/td>\n\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 0<\/td>\n1.5<\/td>\n15<\/td>\n<\/tr>\n
Xanthine oxidase activity (\u00b5kat\/L)<\/strong><\/td>\n5.02\u00b11.83<\/td>\n5.11\u00b11.91<\/td>\n5.43\u00b11.84*<\/td>\n\u00a0\u00a0\u00a0\u00a0\u00a0 5.06\u00b11.72<\/td>\n5.13\u00b11.56<\/td>\n5.64\u00b11.92*<\/td>\n<\/tr>\n
 <\/p>\n

Systolic blood pressure (mmHg)<\/strong><\/td>\n

 <\/p>\n

105\u00b116<\/td>\n

 <\/p>\n

113\u00b112<\/td>\n

 <\/p>\n

138\u00b115*<\/td>\n

 <\/p>\n

108\u00b110<\/td>\n

 <\/p>\n

116\u00b113<\/td>\n

 <\/p>\n

138\u00b112*<\/td>\n<\/tr>\n

 <\/p>\n

Diastolic blood pressure (mmHg)<\/strong><\/td>\n

 <\/p>\n

67\u00b17<\/td>\n

 <\/p>\n

69\u00b19<\/td>\n

 <\/p>\n

74\u00b111<\/td>\n

 <\/p>\n

65\u00b19<\/td>\n

 <\/p>\n

68\u00b116<\/td>\n

 <\/p>\n

76\u00b19*<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Values are expressed as Mean \u00b1SD for n=22 subjects. <\/em><\/p>\n

*P<0.05 compare with the 0hr value. <\/em><\/p>\n

 <\/p>\n

Fifteen hours (15h) after the consumption of ethanol alone or ethanol + fructose, serum xanthine oxidase activity and systemic blood pressure significantly increased (P<0.05) when compared with the basal\u00a0 (0 hr) value (Table 1). Changes induced by ethanol + fructose were higher when compared with levels induced by ethanol.<\/p>\n

Discussion<\/strong><\/p>\n

Fructose administration has been observed to stimulate the oxidation of blood alcohol and consequently reduces intoxication time (Onyesom, 2002).\u00a0 However, present study suggests that such stimulation caused increased xanthine oxidase activity associated with high blood pressure.<\/p>\n

The metabolism of ethanol increases electron flow through the respiratory chain, and this generates reactive oxygen species, (Bailey, et al.<\/em>, 1999) known to produce \u00a0<\/sup>\u00a0\u00a0which stimulates xanthine oxidase activity via suffhydryl oxidation of xanthine dehydrogenase (Houston, et al<\/em>., 1998).<\/p>\n

The stimulation of xanthine oxidase activity results in an increase of juxtaglomerular\u00a0 rennin and decreases nitric oxide, NO (a potent regulator of vasoreactivity) availability (Koppenol, 1998) by\u00a0 repressing macula densa neuronal NO synthase activity (Mazzaili, et al<\/em>., 2001)<\/p>\n

Xanthine oxidase has been implicated as a key oxidative enzyme in the pathogenesis of oxidant \u2013 induced microvascular changes and hypertension (Terada and Willingham, 1991). The administration of fructose to hasten the oxidation of blood alcohol and hence its clearance, may confer high risk of cardiovascular dysfunction and damage, evidence (Table I) suggests.<\/p>\n

The inhibition of xanthine oxidase activity by sodium tungstate enriched diet has been observed to lower microvascular tone and systemic blood pressure (Terada and Willingham, 1991). The administration of fructose to hasten the oxidation of blood alcohol and hence its clearance, may confer high risk of cardiovascular dysfunction and damage. However, the role of sodium tungstate supplemented diet on the associated risk should be verified.<\/p>\n

Acknowledgements<\/strong><\/p>\n

We wish to specially acknowledge Dr. I. Onyesom, whose contributions significantly improved the content of this article.<\/p>\n

References<\/strong><\/p>\n

    \n
  1. Bailey SM, Cunningham CC. (1998). Acute and chronic ethanol increase reactive oxygen species and decrease viability in fresh isolated rat hepatocytes.\u00a0 Hepatology<\/em> 28: 1318 \u2013 1328.<\/li>\n
  2. Bailey SM, Pietsch EC, Cunningham CC. (1999). Ethanol stimulates the production of reactive oxygen species at mitochondrial complexes I and III. Free Radic Biol Med<\/em>. 27: 891 \u2013 900.<\/li>\n
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  8. Onyesom I. (2002). Influence of Oral Fructose on Alcohol \u2013 induced Pathobiochemical changes. Ph.D Thesis, University of Port Harcourt, Nigeria.<\/li>\n
  9. Onyesom I, Anosike EO. (2004). Oral fructose \u2013 induced changes in blood ethanol oxidokinetic data among healthy Nigerians. Southeast Asia J. Trop Med Publ Health<\/em> \u00a035 (2): 476 \u2013 480.<\/li>\n
  10. Peter TJ, Preedy VR. (1998). Metabolic consequences of alcohol ingestion. Norvatis Found Symp<\/em>. 216 : 19 \u2013 24.<\/li>\n
  11. Terada CS, Willingham IR. (1991). Generation of superoxide anion by brain endothelial cell xanthine oxidase. J Cell Physiol<\/em>. 148 : 191 \u2013 196.<\/li>\n
  12. Winer BJ, Brown DR, Michels M. (1991). Design and analysis of single \u2013 factor experiment: completely randomized design. In: Statistical Principles in Experimental Design. McGraw Hill Inc., New York, pp 74 \u2013 418.<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

    Introduction In addition to the oxidation of blood ethanol to […]<\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[10],"tags":[],"class_list":["post-1709","post","type-post","status-publish","format-standard","hentry","category-vol4no1"],"_links":{"self":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/1709","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/comments?post=1709"}],"version-history":[{"count":7,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/1709\/revisions"}],"predecessor-version":[{"id":12936,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/1709\/revisions\/12936"}],"wp:attachment":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/media?parent=1709"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/categories?post=1709"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/tags?post=1709"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}