Biochemical Modulators in Chronic Diseases: The Antioxidant/Anti-Inflammatory Interdependence—2nd Edition

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Pharmaceutical Science".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 815

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Department of Medical Biotechnologies, University of Siena, 53100 Siena, Italy
Interests: lung diseases; chronic obstructive pulmonary disease; oxidative stress biomarkers; pulmonary rehabilitation; sleep disorders and sleep medicine; ozone
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Special Issue Information

Dear Colleagues,

Increasing evidence suggests that inflammation and oxidative stress play a key role in the pathogenesis of many chronic diseases. In fact, oxidative stress underpins the molecular mechanisms responsible for the development of many chronic inflammatory diseases, such as atherosclerosis, diabetes mellitus, chronic obstructive pulmonary diseases, rheumatoid arthritis, and neurodegeneration. Whilst oxidative stress is known to result in an inflammatory response, it has also been suggested that inflammation itself may elicit free radical formation. Reactive oxygen species (ROS) are generated by phagocytic cells, neutrophils, and macrophages during the inflammatory reaction, and chronic infections and inflammatory disorders also provoke an increased production of free radicals. Thus, a close connection has been found to exist between oxidative and inflammatory systems and the development and progression of chronic diseases. It is clear that inflammation and oxidative stress act in unison, exacerbating each other’s effects, leading to a further progression of organ damage. However, the interdependence between these two biochemical pathways is more complex than it appears, as suggested by the lack of clinical trials showing beneficial health effects following the antioxidant treatment of chronic diseases, and by the discovery of the antioxidant paradox. The selection of biochemical agents able to modulate the antioxidant/anti-inflammatory interdependence appears to be a challenge in the prevention and treatment of chronic diseases. This Special Issue provides an overview of the future perspectives of biochemical modulators that act as selective inhibitors along inflammatory and oxidative pathways, as well as the appropriate quantification of both redox and inflammatory status before, during, and after antioxidant or anti-inflammatory therapy. This Special Issue welcomes original research articles, reviews, and short reports on various aspects of antioxidants/anti-inflammatory interdependence in chronic diseases, in addition to the predictions of future trends in related fields.

For access to our previous publications, please visit:

The first volume of this Special Issue: (https://www.mdpi.com/journal/life/special_issues/antioxidant_inflammatory).

Dr. Emma Borrelli
Guest Editor

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Keywords

  • oxidative stress
  • inflammation
  • redox modulator
  • anti-inflammatory agents
  • chronic diseases
  • antioxidant paradox
  • reactive oxygen species

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Published Papers (1 paper)

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Research

27 pages, 5753 KB  
Article
Acrylamide Exposure Exacerbates Type 2 Diabetes-Induced Neurotoxicity: An Integrated Neurobehavioral and Molecular Investigation
by Abdulaziz Arif A. Alshammari, Abdullah Saleh Alkhamiss, Minhajul Arfeen, Razan Alawaji, Mai B. Alwesmi and Vasudevan Mani
Life 2026, 16(3), 491; https://doi.org/10.3390/life16030491 - 17 Mar 2026
Cited by 1 | Viewed by 580
Abstract
Type 2 Diabetes Mellitus (T2DM) is a widespread metabolic disorder that can affect brain health, primarily through the damaging effects of prolonged hyperglycemia. This condition increases oxidative stress (OS), neuroinflammation, and neuroapoptosis, ultimately impairing cognitive function. Acrylamide (ACY), a neurotoxicant formed during high-temperature [...] Read more.
Type 2 Diabetes Mellitus (T2DM) is a widespread metabolic disorder that can affect brain health, primarily through the damaging effects of prolonged hyperglycemia. This condition increases oxidative stress (OS), neuroinflammation, and neuroapoptosis, ultimately impairing cognitive function. Acrylamide (ACY), a neurotoxicant formed during high-temperature food processing and present in cigarette smoke, may further aggravate these neurological disturbances. The present experiment examined the exacerbating effects of T2DM and ACY exposure on cognitive function, neurodegeneration, OS, neuroinflammation, and neuroapoptosis in diabetic rats. T2DM was induced via intraperitoneal injections of nicotinamide and streptozotocin, followed by daily oral doses of ACY for a month. Behavioral assessments (EPM, NOR, and Y-maze) evaluated cognitive performance. Brain tissues were analyzed for biochemical markers of neurodegeneration (GSK-3β, AChE, BACE1), OS (MDA, GSH, Catalase), neuroinflammation (NF-κB, TNF-α, PGE2, COX-2), and neuroapoptosis (Bcl-2, Bax, Caspase-3). Immunohistochemistry of Bcl-2, Bcl-6, CD138, and NF assessed structural brain changes. Results indicated that T2DM and ACY exposure significantly increased the incidence of neurological disturbances. Notably, through increased COX-2, PGE2, MDA, Bax, Bcl-6, Caspase-3, and cognitive decline deficits. This study highlights the harmful neurotoxic amplification of T2DM and ACY exposure, emphasizing the importance of public health measures to reduce ACY exposure through dietary and lifestyle changes, particularly among T2DM populations. Further research into neuroprotective strategies and underlying mechanisms is necessary. Full article
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