Mitochondrial Aging and Metabolism: The Importance of a Good Relationship in the Central Nervous System

The mitochondrial theory of aging suggests that mitochondria have a decrease in production capacity of adenosine triphosphate (ATP). The question may seem trivial, but it becomes more complex when considering that dysfunctional mitochondria can be eliminated by lysosomal digestion and that cell with dysfunctional mitochondria can undergo the process of apoptosis. In organs with regenerative capacity, like the liver, cell proliferation can almost completely hide mitochondrial dysfunction. However, evidence indicates selective damage in mitochondria during aging, and so the mitochondrial aging theory is gaining recognition and respect. There is solid evidence that accumulated DNA damage in mitochondria is a cause directly related to metabolic disorders such as diabetes and degenerative disorders such as Alzheimer’s disease. The central nervous system is particularly susceptible to oxidative damage due to several factors, among which are its high oxygen consumption, its dependence on aerobic carbohydrate metabolism, and its complex composition of membrane lipids. Free radicals are generated at many cell sites, and the mitochondrial respiratory chain is one of the main sources. While many studies have been conducted in experimental animal models, the results are relevant because at least some of their interventions suggest a directing aim at reducing the effects of aging

Oxidative Stress and Parkinson’s Disease: Effects on Environmental Toxicology

Epidemiological studies have found an increased risk of Parkinson’s disease (PD) with environmental factors such as exposure to substances derived from industrial processes, use of agrochemicals, or living in a rural environment. The hypothesis that certain environmental toxins could be the source of the EP is supported by the discovery that chemicals such as herbicides paraquat, diquat, and the fungicide maneb are selectively toxic in nigrostriatal dopaminergic neurons. Also, one of the insecticides produced by plants, such as rotenone, and by-product of the synthesis of synthetic heroin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) can be reproduced in animal models where neurochemicals, histopathological, and clinical characteristic of PD can be found. Interestingly, there are similarities in the chemical structure of paraquat and MPTP. Recent evidence exhibited that inflammation and oxidative stress play an essential role in the development of PD. So, in our laboratory we found that in an animal model melatonin decreases the products of lipid oxidation, nitric oxide metabolites, and the activity of cyclooxygenase 2, which are induced by an intraperitoneal injection of MPTP. This suggests that the neuroprotective effects of melatonin are partially attributed to its antioxidant scavenging and anti-inflammatory action

Physiology and Pathology of Neuroimmunology: Role of Inflammation in Parkinson’s Disease

Parkinson’s disease (PD) is a neurodegenerative disease that affects 1% of the population aged 65 and over and is the second most common neurodegenerative disease next to Alzheimer’s disease. Interneuronal proteinaceous inclusions called Lewy bodies (LB) and a selective degeneration of dopaminergic neurons of the substantia nigra pars compacta (SNPC) are the main features of PD pathology. The most common clinical manifestations are rigidity, tremor, bradykinesia, postural instability, sleep disorders, alterations in gait, smell, memory, and dementia. Genetic and environmental factors are involved in PD, and, recently, oxidative stress, proteasome-mediated protein degradation, and inflammation have acquired relevance as major mechanisms of neuronal dysfunction. Increased levels of reactive oxygen and nitrogen species in the brain contribute to greater vulnerability of proteins to nitro-oxidative modification and to greater degrees of aggregation. These protein aggregates contain a variety of proteins of which α-synuclein appears to be the main structural component. Interestingly, α-synuclein can be secreted by neuronal cells and may lead the initiation and the maintenance of inflammatory events through the activation of microglia, which contributes to dopaminergic neuron depletion. New evidence also suggests that PD may be the result of an autoimmune response in which the immune cells recognize the neurons as foreign elements and would act against them, causing their death

Membrane Fluidity and Oxidative Stress in Patients with Periodontitis

Periodontitis leads to the destruction of dental tissue through polymicrobial interactions, inflammation, and increased oxidative stress. The aim of this study was to measure the levels of nitrates (NO3−), malondialdehyde (MDA), and membranal fluidity (MF) in the gingival tissue of subjects with or without periodontitis. A total of 120 participants from the Dentistry School of the University of Guadalajara were investigated. The study was approved by the ethics committee of our institution, with the registration number of CI-01221. The clinical parameters measured were probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BoP). NO3− was measured using the Greiss reaction, while MDA was determined colorimetrically with the FR12 Kit (Oxford Biomedical Research). Membrane fluidity (MF) was measured using the quotient Ie/Im according to the method of Ortiz and collaborators. The Student t-test, Spearman correlation, and chi-square are used to calculate the results. The results showed higher levels of PD, CAL, and BoP in patients. There was a positive correlation between MF and PD. Moreover, MDA was positively correlated with PD and CAL. Increases in PD resulted in higher levels of NO3−, MDA, and MF. Similarly, increases in CAL resulted in higher levels of MDA and MF in patients. We conclude that PD and CAL facilitated the progression of periodontitis through increases in MDA and MF