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Effects of selenium toxicity and deficiency on humans

 

Table Of Contents


Chapter ONE

1.1 Introduction
1.2 Background of Study
1.3 Problem Statement
1.4 Objective of Study
1.5 Limitation of Study
1.6 Scope of Study
1.7 Significance of Study
1.8 Structure of the Research
1.9 Definition of Terms

Chapter TWO

2.1 Introduction to Literature Review
2.2 Overview of Selenium
2.3 Sources of Selenium
2.4 Selenium Toxicity in Humans
2.5 Selenium Deficiency in Humans
2.6 Health Implications of Selenium Toxicity
2.7 Health Implications of Selenium Deficiency
2.8 Selenium in Medical Research
2.9 Selenium in Nutrition Studies
2.10 Comparative Studies on Selenium Effects

Chapter THREE

3.1 Introduction to Research Methodology
3.2 Research Design
3.3 Sampling Techniques
3.4 Data Collection Methods
3.5 Data Analysis Procedures
3.6 Ethical Considerations
3.7 Research Validity and Reliability
3.8 Limitations of the Methodology

Chapter FOUR

4.1 Introduction to Discussion of Findings
4.2 Analysis of Selenium Toxicity Effects
4.3 Analysis of Selenium Deficiency Effects
4.4 Comparison of Toxicity and Deficiency Findings
4.5 Recommendations for Selenium Intake
4.6 Public Health Implications
4.7 Future Research Directions
4.8 Conclusion of Findings Discussion

Chapter FIVE

5.1 Conclusion and Summary
5.2 Recap of Research Objectives
5.3 Key Findings Summary
5.4 Contributions to Existing Knowledge
5.5 Implications for Future Studies

Project Abstract

Abstract
Selenium is an essential trace element that plays a crucial role in various physiological processes in the human body. Both selenium toxicity and deficiency can have significant impacts on human health. This review aims to provide an overview of the effects of selenium toxicity and deficiency on humans. Selenium toxicity can occur when the intake of selenium exceeds the tolerable upper intake level. Acute selenium toxicity can result in symptoms such as nausea, vomiting, abdominal pain, and fatigue. In severe cases, it can lead to respiratory distress, heart failure, and even death. Chronic selenium toxicity is rare but can cause symptoms like hair and nail loss, skin lesions, and neurological abnormalities. Conversely, selenium deficiency is more common and can have serious health consequences. Selenium is a key component of selenoproteins, which have antioxidant properties and play a role in thyroid hormone metabolism, immune function, and reproduction. Inadequate selenium intake can lead to an increased risk of various health conditions, including cardiovascular disease, cancer, and infertility. Selenium deficiency has been associated with Keshan disease, a potentially fatal form of cardiomyopathy, as well as Kashin-Beck disease, a type of osteoarthritis. The effects of selenium toxicity and deficiency are mediated through multiple mechanisms. Selenium is involved in redox reactions as part of selenoproteins like glutathione peroxidases and thioredoxin reductases. Both excess and insufficient selenium levels can disrupt redox balance, leading to oxidative stress and cellular damage. Selenium toxicity can also interfere with the metabolism of other trace elements like zinc and copper. Assessing selenium status in individuals can be challenging due to variations in selenium content in soil and food sources. Biomarkers such as plasma selenium levels and selenoprotein activity are used to evaluate selenium status. Treatment strategies for selenium toxicity involve discontinuing selenium exposure and providing supportive care, while selenium deficiency can be addressed through dietary supplementation or food fortification. In conclusion, maintaining optimal selenium levels is crucial for human health. Both selenium toxicity and deficiency can have detrimental effects on various physiological processes. Further research is needed to better understand the mechanisms underlying the effects of selenium imbalance and to develop effective strategies for preventing and managing selenium-related health conditions.

Project Overview

INTRODUCTION

1.1.          BACKGROUND INFORMATION

Selenium (Se) is an essential trace element having biological functions of utmost importance for human health. Different from the other (semi) metals, it is incorporated into proteins by a co-translational mechanism as part of the amino acid selenocysteine (SeCys), the 21st amino acid used for protein synthesis in humans, whereas only a few of them have been functionally characterized. Most Se-proteins participate in antioxidant defence and redox state regulation, particularly the families of more specific essential roles, such as iodothyronine deiodinases (DIOs) which are involved in thyroid hormones metabolism, GPx4 which is essential for spermatogenesis, and selenophospathe synthetases 2 (SPS2) participating in Se-protein biosynthesis.

Other Se-proteins may be involved in important biological processes, but their exact mechanism of action is still yet to be fully understood. Despite the scarce knowledge of the precise biochemical functions, a very large number of studies have been carried out in the last two decades showing that insufficient Se levels, and particularly Se-proteins, are associated with several human diseases including cancer, diabetes, cardiovascular and immune system disorders. In most cases, the link lies in the contrast to the oxidative stress that may be booth causing or caused by the disease. In this context, it is important to decipher whether and adequate Se status may contrast the risk factors for health disorders, or Se supplementation may improve the therapy when Se metabolism is altered.

Despite many studies that have suggested a beneficial effect from Se supplementation to general health protection, most of them have remarked that it is limited to general health protection, most of them have remarked that it is limited to the initially inadequate Se status. Conversely, care should be taken when using supplements because excessive Se intake leads to toxic effects, and recent studies have shown that even sub-toxic doses may be negatively impacting, for example by increasing the risk of type 2 diabetes.


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