Sixty percent of global agricultural production depends on the use of pesticides, despite their adverse effects on human health and the ecosystem. In Mexico, the application of these products has been exacerbated, including pesticides already banned in other countries. The objective of this study was to determine pesticide concentrations in samples of water purification plants and surface water from the Cienega area of Jalisco, Mexico. A survey of 119 farmers with occupational exposure to pesticides was carried out in order to obtain information on the most frequently used pesticides. Subsequently, 51 samples taken at 7 different sites were analyzed using liquid chromatography and mass-mass spectrometry. The most frequently used pesticides were organophosphates (28.87%), pyrethroids (12.89%), and the herbicide paraquat (31.95%). In surface water, the prevalent pesticides were glyphosate (56.96–510.46 ppb) and malathion (311.76–863.49 ppb). Glyphosate levels were higher than the limits acceptable in daily water intake in Cumuato. Malathion levels exceeded the limits permissible by EPA in water purification plants in urban public establishments (100 ppb for children, and 200 ppb for adults). In addition, a multidimensional scaling analysis showed that the sampled sites could be grouped into 2 different bodies of water, based on similarities in their glyphosate concentrations (stress = 0.005), while the concentrations of malathion were heterogeneous (stress = 0.001).

Melatonin, N-acetyl-5-hydroxytryptamine, is a hormone that synchronizes the internal environment with the photoperiod. It is synthesized in the pineal gland and greatly depends on the endogenous circadian clock located in the suprachiasmatic nucleus and the retina’s exposure to different light intensities. Among its most studied functions are the regulation of the waking-sleep rhythm and body temperature. Furthermore, melatonin has pleiotropic actions, which affect, for instance, the modulation of the immune and the cardiovascular systems, as well as the neuroprotection achieved by scavenging free radicals. Recent research has supported that melatonin contributes to neuronal survival, proliferation, and differentiation, such as dendritogenesis and axogenesis, and its processes are similar to those caused by Nerve Growth Factor, Brain-Derived Neurotrophic Factor, Neurotrophin-3, and Neurotrophin-4/5. Furthermore, this indolamine has apoptotic and anti-inflammatory actions in specific brain regions akin to those exerted by neurotrophic factors. This review presents evidence suggesting melatonin’s role as a neurotrophic factor, describes the signaling pathways involved in these processes, and, lastly, highlights the therapeutic implications involved.

Background: Heavy metals such as mercury (Hg), lead (Pb) and arsenic (As) are elements that promote the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) involved in the etiology of oxidative stress. They cause oxidative damage to membrane lipids, proteins and DNA, thereby activating pathways of apoptosis and tissue degeneration. Some chemical species derived from these metals include methyl mercury (CH3Hg+), tetraethyl lead [(CH3CH2)4Pb], arsenate (AsO43-) and arsenite (AsO2-), all of which have the capacity to induce oxidative stress and renal damage. Purpose: To comprehensively review the effects of Hg, Pb, As and Zinc (Zn) on renal oxidative status. Methods: Literature survey was done using key words such as heavy metals, oxidative stress and kidney damage using search engines for free scientific publications such as PubMed database, FreeFullPDF.com and Google Scheler. Results: It was revealed that Hg, Pb and As contribute significantly to oxidative stress by stimulating the generation of free radicals, oxidation of biomolecules, deregulation of pro-oxidant proteins, and activation of pro-inflammatory molecules, which ultimately lead to renal damage. There is a strong association between exposure to these heavy metals and chronic renal damage, since their bioaccumulation deregulates glomerular filtration and tubular secretion due to excessive production of ROS and activation of apoptotic pathways. However, studies have shown that Zn possesses renoprotective and antioxidant effects, and its deficiency leads to oxidative stress. Conclusion: The results of this survey suggest that deficiencies of Hg, Pb, As and Zn produce different degrees of oxidative damage which negatively impact on renal health.

Pesticides are chemical substances used to control, prevent, or destroy agricultural, domestic, and livestock pests. These compounds produce adverse changes in health, and they have been associated with the development of multiple chronic diseases. This study aimed to present a detailed review of the effect of pesticides on the oral cavity and the oral microbiome. In the oral cavity, pesticides alter and/or modify tissues and the microbiome, thereby triggering imbalance in the ecosystem, generating an inflammatory response, and activating hydrolytic enzymes. In particular, the imbalance in the oral microbiome creates a dysbiosis that modifies the number, composition, and/or functions of the constituent microorganisms and the local response of the host. Pesticide exposure alters epithelial cells, and oral microbiota, and disrupts the homeostasis of the oral environment. The presence of pesticides in the oral cavity predisposes the appearance of pathologies such as caries, periodontal diseases, oral cancer, and odontogenic infections. In this study, we analyzed the effect of organochlorines, organophosphates, pyrethroids, carbamates, bipyridyls, and triazineson oral cavity health and ecosystems.

Background: The region of La Cienega in Jalisco Mexico, is an important agricultural reference for the production of corn, sorghum and wheat, among other grains, so the use of pesticides for pest control is high. However, in this rural area there are no toxicological studies that assess the occupational risk of pesticide use. Therefore, this study is the first to determine the oxidative stress levels markers (GSH, GSSG, carbonyl groups, nitric oxide metabolites and lipid peroxides) as well as alteration of the mitochondrial membrane fluidity caused by occupational exposure to organophosphorus and carbamates in farmers of this region. This occupational risk can increase cellular oxidation, which explains the high prevalence of neurodegenerative diseases and cancer in Cienega settlers to be analyzed in future studies. Methods: Comparative cross-sectional study was performed using two groups: one not exposed group (n = 93) and another one with occupational exposure (n = 113). The latter group was sub-divided into 4 groups based on duration of use/exposure to pesticides. Oxidative stress levels and membrane fluidity were assessed using spectrophotometric methods. Statistical analyses were performed using SPSS software ver. 19.0 for windows. Results: The most commonly used pesticides were organophosphorus, carbamates, herbicide-type glyphosate and paraquat, with an average occupational exposure time of 35.3 years. There were statistically significant differences in markers of oxidative stress between exposed farmers and not exposed group (p = 0.000). However, in most cases, no significant differences were found in markers of oxidative stress among the 4 exposure sub-groups (p > 0.05). Conclusion: In the Cienega region, despite the indiscriminate use of organophosphorus and carbamates, there are no previous studies of levels oxidative stress. The results show increased levels of oxidative stress in occupationally exposed farmers, particularly membrane fluidity levels increased three times in contrast to not exposed group.

Demyelinating diseases alter myelin or the coating surrounding most nerve fibers in the central and peripheral nervous systems. The grouping of human central nervous system demyelinating disorders today includes multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD) as distinct disease categories. Each disease is caused by a complex combination of genetic and environmental variables, many involving an autoimmune response. Even though these conditions are fundamentally similar, research into genetic factors, their unique clinical manifestations, and lesion pathology has helped with differential diagnosis and disease pathogenesis knowledge. This review aims to synthesize the genetic approaches that explain the differential susceptibility between these diseases, explore the overlapping clinical features, and pathological findings, discuss existing and emerging hypotheses on the etiology of demyelination, and assess recent pathogenicity studies and their implications for human demyelination. This review presents critical information from previous studies on the disease, which asks several questions to understand the gaps in research in this field.