Beer Intake Reduces Gene Expression Of Tumors Research Papers Examples

Type of paper: Research Paper

Topic: Beer, Experiment, Aluminum, Community, Cancer, Information, Alcoholism, Education

Pages: 7

Words: 1925

Published: 2020/11/25

Introduction

Experimental and epidemiological researches have pointed that diet and environmental factors significantly determines the likelihood of tumors or human cancer. Even though the genetic history of people may influence the chance of neoplastic disease, it is still not the prevailing value in the preponderance of circumstances. Awareness has to be agreed to daily diet with chemo-preventive actions to diminish the risk of cancer. Studies have shown that alcohol consumption is associated with death from cancer. The relation of the risk to mortality reduces for moderate drinkers in contrast to nondrinkers and then amplifies with elevated alcohol drinking.
Beer along with wine polyphenols and alcohol has been linked with diet in many different countries. Regular and moderate use of beer has been believed to have health benefits. According to Arranz, et al. (2012), various researches established that drinking of alcoholic beverages creates helpful effects on the coagulation system, lipid profile and capacity of antioxidant that is good for human health. On the contrary, binge or alcohol abuses pose plenty of negative effects including work, social and medical related problems.
Positive effects of light and moderate consumption of beer have been documented on cognitive function, cellular aging damage and dementia. The good effects of beer intake are attributed to its anti inflammatory and antioxidants effects. The components of beer such as polyphenols are anticarcenogenic, hypotensive, antioxidant and anti-inflammatory .
This paper aims to present two scientific papers that discuss about beer intake reducing gene expression of tumors and give an argument about which scientific research paper presented the topic better. The argument will be based on the type of data presented, the control groups, number of subjects in the experiment and the variable and overall design of the experiment.
The two scientific research paper that was chosen to be discussed in this paper are entitled “Beer Consumption Reduces Cerebral Oxidation Caused by Aluminum Toxicity by Normalizing Gene Expression of Tumor Necrotic Factor Alpha and Several Antioxidant enzymes” by Gonzalez-Munoz et al., (2008), and “Intake of Beer Inhibits Azoxymethane-Induced Colonic Carcinogenesis in Male Fischer 344 Rats” by Nozawa, et al. (2004).
Beer Consumption Reduces Cerebral Oxidation Caused by Aluminum Toxicity by Normalizing Gene Expression of Tumor Necrotic Factor Alpha and Several Antioxidant Enzymes by Gonzalez-Munoz, Meseguer, Sanchez-Reus, Schultz, Olivero, & Benedi (2008)
The research investigated the effect of silicon consumed as beer or silicic acid on inhibiting toxic effect of aluminum inside the brain. This probability relies on the assumption that beer consumption can normalize gene expression of tumor. Neurotoxicity caused by aluminum (Al) is well recognized and diverse aluminum salts have been accounted to hasten oxidative impairment to biomolecules.
The study used the reagents including silicic acid, Si(OH) or SiO2 and Aluminum nitrate [Al(NO3)3 * 9H2O] . The reagents used were of the premier quality accessible and attained from marketable supplies. Dissolved silicic acid in saline solution (0.9%) and ethanol (2%) and Al nitrate in saline (0.9%) was used. The chemicals were administered through the mouth at a 0.5 mL volume.
On the other, the subjects of the experiment are six week old male NMRI mice. The animals, obtained from the University of Alcala Animal Research Center, weigh about 30 g. The Ministerio de Agricultura in Spain homologated the subjects. They were kept inside a room under standard temperature and humidity. The room is also exposed with a twelve-hour light and dark succession. The experiment complies with the safeguard of scientific research animals. The experiment used twelve rats which are categorized into four subgroups. The control group is composed of mice getting deionized water only. The remaining mice from the other groups get 450 lg/ml aluminum nitrate, Al(NO3)3* 9H2O dissolved in deionized water through their drinking water. The intoxicated mice get aluminum nitrate while the other groups received a 50 mg/ml solution of silicic acid and aluminum nitrate and dose of aluminum nitrate and (5.5% alcohol by volume) commercial beer.
The results of the experiment showed that the aluminum brain levels of the group of mice that received aluminum nitrate were four times higher compared to those of the control mice. On the other hand, the mice group that received aluminum nitrate and silicic acid solution as well as the group of mice that received aluminum nitrate and commercial beer were 40% lower of aluminum brain level compared to those of the group that received aluminum nitrate.
The research has observed that the beer prohibited the buildup of lipid damage considerably, because of the aluminum drinking. The beer and the silicic acid also inhibited the decline on the expression of endogenous antioxidant enzymes mRNA related with aluminum intake.
The RNA expression of tumor necrosis factor alpha (TNFa) was standardized in beer groups and silicic acid groups. The study determined extremely high and noteworthy relationships for the diverse parameters experimented. This implies that modest utilization of beer, because of its silicon content, successfully defends the body against the harmful effects of neurotoxic in aluminum.
“Intake of Beer Inhibits Azoxymethane-Induced Colonic Carcinogenesis in Male Fischer 344 Rats” by Nozawa et al., (2004)
This study investigated the effects of beer drinking on azoxymethane (AOM). Azoxymethane induced colonic Aberrant Crypt Foci (ACF) in rats, and it has been utilized to recognize chemical factors that put off colon cancer, counting numerous dietary aspects particularly those obtained from plant resources.
The experiment used male Fischer 344 rats with the age of four weeks. They were from Charles River Japan and were kept inside wire cages within an air-conditioned area with constant temperature and humidity. The rats are permitted to have right to use to a basal diet. After four days of acclimatization, the rats underwent a randomization to separate them into groups.
The study used the method of electrophoresis assay employing single cell gel. Rats fed with extract from beer or malt for two weeks showed a significant reduction on the colonocytes of DNA damage which is brought on by a sole AOM injection with concentration of 15 mg per kg body mass. AOM also induced the ACF formation in the mucosa of the colon. The investigation of the ACF showed that feeding beer on the duration of five weeks also reduced the quantity of ACF by thirty-five percent.
Twenty-six percent reductions in ACF formation are not significant in the post-instigation procedure. Another observation was that different brands of beer also resulted to varied efficiency of ACF formation inhibition. Freeze-dried Beer (FD Beer) reduced the ACF formation considerably while ethanol did not reduce the formation. This implies that the nonvolatile compositions of the beer are accountable for the decline of formation.
On the other hand, the group of rats that is treated with hot water extract of malt, particularly with colored malts extracts, showed a considerable inhibition of ACF formation. The group of rats fed with hops extract did not show any sign of reduction.
Forty-two weeks of experimentation resulted to 22% reduction of tumor incidence due to beer intake. Beer intake also reduced the cases of neoplastic lesions such as adenomas and adenocarcinomas to about 44%.
The results of the experiment imply that beer consumption can reduce the risk of cancer vulnerability, and the components of beer prevent chemo effects on AOM-induced colonic carcinogenesis.
Comparison of the Two Research Papers Based On Type of Data Presented; the Control Groups; the Number of Subjects in the Experiment; the Variable and Overall Design of the Experiment
The first research paper presented the data obtained through tables with corresponding discussions. The analytical method used inductively coupled plasma atomic emission spectrometry measuring method. Using an Uvikon 930 spectrophotometer, biochemical assays were measured and the reverse amplification and transcription by means of the Titan system was used to obtained an RT-PCR real time analysis. The statistical analysis, on the other hand, was done in triplicate. Data were presented median (from minimum to maximum) and as means ± SD. A non-parametric test using Kruskal–Wallis was employed subsequently to several non-parametric evaluation tests. To observe the relationship between TBARS and aluminum and the diverse antioxidant enzyme expressions and TNFa, spearman correlations were done. Statistical analyses used the SAS (version 9.1) and the SPSS statistical software package (version 13.0). On the other hand, the second research article used graphs and table to present the data obtained from the experiment. The experiment used the method of single cell gel electrophoresis assay and for the statistical analysis, the data presented as means±SD. One-way ANOVA was used to analyze the data in the ACF experiment and in the comet assay. Subsequent to it are the Kruskal-Wallis or Dunnett’s test followed by the Bonferroni Correction. Comparison between the tumor multiplicity and ACF in the enduring investigation was done through the Mann- Whitney-U-test. The tumor incidence was evaluated using Fischer’s exact probability test and X2 test. For the two research articles, the Significant differences were considered when p <0.05.
The data presented in the first research article can be considered as the better one between the two since it utilized statistical analysis in triplicates and also presented both the mean and the median of the data. Moreover, the first research article utilized both a parametric and non-parametric method of analysis .
The control group in the first article is consists of mice that got only deionized water while the control group in the second article is consist of rats fed with water. The total number of subjects in the first article is twelve and is divided into four groups. The control group in this experiment is consisted of mice that received only deionized water while the three experimented group received aluminum nitrate dissolved in water. The variable in the experiment is the component of the substance being fed to the mice. The first experimental group received only aluminum nitrate, the second group received aluminum nitrate and silicic acid, and the last group received aluminum nitrate and beer. The experiment lasted for three months.
On the other hand, the long term experiment in the second article employed ninety-three rats that were at random divided into three groups. The three groups consist of the AOMwater group (40 rats), the AOM_beer group (40 rats) and the AOM untreated group (13 rats). The variable in the experiment is also the components of the substance they received. The AOM_water and beer groups got subcutaneous shot of AOM while the untreated group received saline water injection. The experiment lasted for forty-two weeks.
In terms of the control groups, number of subjects, variable as well as the duration of the study, we can observe that the second article is better than the first. This is because the number of subjects is greater which can provide reliable data and conclusion. Although the two experiments have the same variable, which is the components of the substances being fed to the subjects, the second article used an experimental sample of beer unlike the first study that used commercially purchased beer. The second article is better because it has the control over the exact components of the beer being fed to the rats. Another advantage of the second article is the duration of the experiment (42 weeks) compare to the first research article (12 weeks). Longer period of experiment presents a more reliable data on the likelihood of tumor or cancer formation or carcinogenesis .
The overall design of the experiment of the second research paper is also better than the first research paper presented. First, it involves production of experimental samples; beers and ethanol content was controlled to attain a homogenous condition of feeding the subjects. This method, as mentioned before is better than the first paper in which the substances being fed are just bought commercially. Then in the second research, the subjects were classified into three group, base on the kind of diet/ injection they received, which are composed of forty rats for the two groups and thirteen rat for the controlled group. Unlike the first article that divided their subjects into four groups, also based on the diet they received, which are composed of only three mice each group. The second research definitely poses a more reliable basis of data in terms of number of subjects. Lastly, the second article further divided their subjects into different protocols upon investigation of ASC formation which gives a more detailed and comprehensible interpretation and analysis of the results .

References

Arranz, S., Chiva-Blanch, G., Valderas-Martínez, P., Medina-Remón, A., Lamuela-Raventós, R. M., & Estruch, R. (2012). Wine, Beer, Alcohol and Polyphenols on Cardiovascular Disease and Cancer. Nutrients , 4, 759-781.
Bird, R. P. (1987). Observation and quantification of aberrant crypts in the murine colon treated with a colon carcinogen: preliminary findings. Cancer Lett , 147–51.
Gonzalez-Munoz, M., Meseguer, I., Sanchez-Reus, M., Schultz, A., Olivero, R., & Benedi, J. (2008). Beer consumption reduces cerebral oxidation caused by aluminum toxicity by normalizing gene expression of tumor necrotic factor alpha and several antioxidant enzymes. Food and Chemical Toxicology , 46, 1111–1118.
Hollander, M., & Wolfe, D. (1973). Nonparametric Statistical Method. New York: Wiley.
Nozawa, H., A. Y., Tajima, O., Katayama, M., Sonobe, H., Wakabayashi, K., et al. (2004). Intake of Beer Inhibits Azoxymethane-Induced Colonic Carcinogenesis in Male Fischer 344 Rats. Int. J. Cancer , 108, 404–411.
Wargovich, M., Jimenez, A., McKee, K., Steele, V., Velasco, M., Woods, J., et al. (2000). Efficacy of potential chemopreventive agents on rat colon aberrant crypt formation and progression. Carcinogenesis , 1149–55.

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