Antioxidants: Chemistry, Natural Sources and Health Benefits | Chapter 8 | Disease and Health: Research Developments Vol. 8

Antioxidants are a class of compounds that play a crucial role in maintaining human health and preventing diseases. They are found in a wide range of natural sources, including fruits, vegetables, nuts, and seeds. Antioxidants are also synthesized in the human body, where they help to protect cells from damage caused by free radicals. Chemically, antioxidants are a diverse group of compounds that share the ability to neutralize or mop up free radicals. Free radicals are highly reactive molecules that are formed in the body as a result of normal metabolic processes, exposure to environmental stressors, and other factors. If left unchecked, free radicals can cause oxidative stress, which can lead to cell damage, inflammation, and a range of chronic diseases. Antioxidants work by donating electrons to free radicals, thereby neutralizing their reactivity and preventing them from causing harm to cells and tissues. Different antioxidants have different mechanisms of action, and some may be more effective than others in preventing specific types of cell damage. The health effects of antioxidants are numerous and well-documented. A diet rich in antioxidants has been shown to reduce the risk of chronic diseases such as heart disease, cancer, and cognitive decline. Antioxidants may also help to improve immune function, reduce inflammation, and promote healthy aging. Some of the most well-known antioxidants include vitamins C and E, beta-carotene, and other carotenoids, as well as polyphenols such as flavonoids and phenolic acids. Other antioxidants, such as selenium and zinc, are important minerals that play a crucial role in maintaining antioxidant defenses in the body.

Author (s) Details

 

Oluranti Olagoke Ogunmola
Department of Chemistry, Emmanuel Alayande University of Education, Oyo, Nigeria.

 

Mumini Adekunle Amusat
Department of Biology, Emmanuel Alayande University of Education, Oyo, Nigeria.

 

Kingsley Oyediran Oke
Department of Biology, Emmanuel Alayande University of Education, Oyo, Nigeria

Sodamade A.
Department of Chemistry, Emmanuel Alayande University of Education, Oyo, Nigeria.

 

Please see the book here:- https://doi.org/10.9734/bpi/dhrd/v8/4877

Insulin Resistance Contributes to Neuroinflammation, Cognitive Decline and Brain Senescence in Congenic Obese LA/Ntul//-cp Rats | Chapter 9 | Advancement and New Understanding in Medical Science Vol. 7

Search for a suitable an animal model may prove to be more productive to determine if insulin resistance and its direct metabolic sequelae might be significant co-contributors to the neuronal declines that occur in NIDDM, obesity, and progression of dementia conditions. The burgeoning prevalence of obesity and overweight conditions from the age of adolescence and throughout the lifespan has reached epidemic proportions in industrialized nations throughout the globe. One of the most prevalent findings in obesity is the emergence of insulin resistance, which is linked to both a persistent inflammatory state and systemic hypoxia in adipose tissue. Insulin resistance impacts several aspects of substrate oxidation and oxidative free radical production in brain and somatic tissues, and it is likely that adipose tissue depots are the source of cytokine-linked chronic inflammation. In studies with aging congenic lean and obese rats chronic hyperinsulinemia and brain shrinkage has now been reported, albeit it in the absence of Type 2 diabetes (NIDDM), hypertension (HTN) or other comorbidities, thereby suggesting that aspects of disordered substrate metabolism including insulin resistance as commonly observed in obesity may be a key contributory factor in the development of a neuroinflammatory linked brain shrinkage with accompanying decreases in brain mass, protein and DNA content, and which were further compromised when fed an isocaloric high vs. a low glycemic insulinogenic diet containing sucrose vs. cornstarch respectively. These findings imply that in this strain of obese rats, chronic insulin resistance due to obesity, which is at least partially caused by dietary variables, is a plausible independent risk factor in the development of neuroinflammation, DNA damage, brain shrinkage, and neural senescence.

Author(s) Details:

Orien L. Tulp,
Colleges of Medicine and Graduate Studies, University of Science Arts and Technology, Montserrat, British West Indies, MSR1110 and the Einstein Medical Institute, North Palm Beach, FL 33409, USA.

Please see the link here: https://stm.bookpi.org/ANUMS-V7/article/view/13427