Mercury (Hg) is one of the toxic metals of global and environmental concern, with aquatic Hg cycling being central in determining the production of highly toxic methylmercury and the air-water Hg exchange influencing the long-range intercontinental atmospheric Hg transport. Both inorganic and organic forms of Hg can be bound by suspended particles, including inorganic minerals (in particular metal oxides/sulfides) and particulate organic matter. Photochemical transformation is a critical process in surface water, and the role of suspended particles in Hg redox photoreactions has increasingly emerged, albeit in limited studies in comparison to extensive studies on aqueous (homogeneous) photoreactions of Hg. The lack of understanding of what roles suspended particles play might result in inaccurate estimation of how Hg species transform and/or cycle in the environment. In view of this gap, this paper critically reviews and synthesizes information on the studies conducted on different natural surface waters with respect to the potential roles of suspended particles on Hg photo-redox reactions. It robustly discusses the various possible pathways and/or mechanisms of particle-mediated Hg (II) reduction, in enhancing or lowering the production of dissolved gaseous mercury. These processes include photo hole-electron pair formation and reactive oxygen species generation from particle excitation and their involvement in Hg photoreduction, in addition to the light attenuation effect of particles. This paper highlights the necessity of future studies exploiting these particles-mediated Hg photoreactions pathways and the implications of including these heterogeneous photoreactions (together with particulate elemental Hg species) on the air-water Hg exchange estimation.

The explosive compound 2,4,6-trinitrotoluene (TNT) is well known as a major component of munitions. In addition to its potential carcinogenicity and mutagenicity in humans, recent reports have highlighted TNT toxicities in diverse organisms due to its occurrence in the environment. These toxic effects have been linked to the intracellular metabolism of TNT, which is generally characterised by redox cycling and the generation of noxious reactive molecules. The reactive intermediates formed, such as nitroso and hydroxylamine compounds, also interact with oxygen molecules and cellular components to cause macromolecular damage and oxidative stress. The current review aims to highlight the crucial role of TNT metabolism in mediating TNT toxicity, via increased generation of reactive oxygen species. Cellular proliferation of reactive species results in depletion of cellular antioxidant enzymes, DNA and protein adduct formation, and oxidative stress. While TNT toxicity is well known, its ability to induce oxidative stress, resulting from its reductive activation, suggests that some of its toxic effects may be caused by its reactive metabolites. Hence, further research on TNT metabolism is imperative to elucidate TNT-induced toxicities.

UNASSIGNED: Pulmonary tuberculosis (PTB) is a major public health concern in most underdeveloped and developing countries. PTB affects the nutritional status of the patients and influences the body mass index (BMI). There is tissue inflammation and free radical burst from activated phagocytes resulting in oxidative stress. The present study was designed to assess the relationship between oxidative stress and body mass index in newly detected pulmonary tuberculosis patients.
UNASSIGNED: This was a case-control study designed to assess oxidative stress parameters such as nitric oxide (NO) and malondialdehyde (MDA) in 40 consecutives newly diagnosed PTB patients and compared with 40 age-matched healthy controls. The nutritional status of the study subjects was measured by calculating the BMI.
UNASSIGNED: The mean BMI was 21.61±3.52 Kg/m2 in controls and 17.47±1.56 Kg/m2 in PTB patients and the difference was statistically significant (p <0.0001). The mean levels of MDA (7.65±0.65 nmol/ml) and NO (36.12±1.07 μmol/l) were significantly higher in PTB patients compared to controls (MDA 3.56±0.41 nmol/ml and NO 14.48±0.93 μmol/l).
UNASSIGNED: Increased levels of malondialdehyde and nitric oxide were observed in newly diagnosed PTB patients when compared to controls indicating oxidative stress in PTB. The BMI of these patients was significantly lower than the controls. Thus, it is concluded that there is an inverse relationship between oxidative stress and BMI in PTB patients and antioxidant supplementation in addition to nutritional intervention under the National Tuberculosis Elimination Program may help to improve the BMI and promote better recovery in these patients.

Cancer is one of the most significant causes of death worldwide. Despite the rapid development of modern forms of therapy, results are still unsatisfactory. The prognosis is further worsened by the ability of cancer cells to metastasize. Thus, more effective forms of therapy, such as photodynamic therapy, are constantly being developed. The photodynamic therapeutic regimen involves administering a photosensitizer that selectively accumulates in tumor cells or is present in tumor vasculature prior to irradiation with light at a wavelength corresponding to the photosensitizer absorbance, leading to the generation of reactive oxygen species. Reactive oxygen species are responsible for the direct and indirect destruction of cancer cells. Photodynamically induced local inflammation has been shown to have the ability to activate an adaptive immune system response resulting in the destruction of tumor lesions and the creation of an immune memory. This paper focuses on presenting the latest scientific reports on the specific immune response activated by photodynamic therapy. We present newly discovered mechanisms for the induction of the adaptive response by analyzing its various stages, and the possible difficulties in generating it. We also present the results of research over the past 10 years that have focused on improving the immunological efficacy of photodynamic therapy for improved cancer therapy.

The road between a hypothesis about a disease or condition and its cure or palliation is never simply linear. There are many tantalizing tangents to be chased and many seemingly obvious truths with countless exceptions; this is usually a feature, not a bug, as they say in computer programming. In the tangents and exceptions are clues and alternative roads to science and medicine that can provide cures and palliative measures, sometimes for diseases or conditions other than the one being studied. The narrative that follows uses the author\'s scientific experience in childhood nervous system cancer to illustrate the importance of a robust, bidirectional interaction between the laboratory bench and the clinic bedside in the quest for solutions to problems of health, longevity, and quality of life.

BACKGROUND: The antioxidant enzymes are important cellular components involved in detoxification of reactive oxygen species (ROS) and protect cells from ROS induced oxidative damage. Single nucleotide polymorphisms (SNPs) of antioxidant enzyme coding genes such as superoxide dismutase (SOD) and catalase (CAT) may alter the enzyme activity which can influence susceptibility towards carcinogenesis.  Therefore, the present study was planned to investigate possible SNPs of SOD (SOD1 (Cu,Zn-SOD), SOD2(Mn-SOD), SOD3(EC-SOD) and CAT genes and their possible association with breast cancer risk in rural Indian women.
METHODS: In this case-control study, the association of SOD and CAT gene polymorphism was studied by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The study was conducted among 400 clinically breast cancer patients and 400 healthy women in a population of South-Western Maharashtra. The logistic regression analysis was carried out to calculate Odds ratio (OR) with 95% confidence interval and p-value, where p ≤0.05 was considered as statistically significant.
RESULTS: The results of analysis of genotype frequency distribution showed significant association of rs4880 SNP of Mn-SOD with BC risk at homozygous variant (CC/CC) genotype (OR 2.46; 95%CI, 1.61-3.75; p<0.0001) and corresponding frequency of variant (C) allele (OR 1.53; 95%CI, 1.25-1.86; p<0.0001). In CAT gene polymorphisms the variant (T/T) was increased significantly in BC cases as compared to controls (OR 3.45; 95%CI, 2.17-5.50; p<0.0001) along with its variant (T) allele (OR 2.01; 95%CI, 1.63-2.48; p<0.0001).
CONCLUSIONS: The results implied that, C/C genotype of SOD2-1183T/C polymorphism and T/T genotype of CAT-262 C/T polymorphism may be associated with an increased breast cancer risk. However, SOD1-251 A/G and SOD3-172 G/A polymorphisms did not show any significant difference in variant homozygous genotypes of patients compared to controls.

Reset osmostat syndrome (ROS) is characterized by a change of normal plasma osmolality threshold (decrease or increase), which leads to chronic dysnatremia (hypo- or hypernatremia). We have described a clinical case of ROS and chronic hyponatremia in a patient with chordoid glioma of the III ventricle. It is known that the patient had previously been diagnosed with hyponatremia (131-134 mmol/l). She has not hypothyroidism and hypocorticism. There is normal filtration function of the kidneys was (CKD-EPI 91.7 ml/mi/1,73m2). Urine osmolality and sodium level were studied to exclude of concentration kidney function disorder. During first three days after removal of the tumor of the third ventricle (chordoid glioma, WHO Grade II), the sodium level decreased to 119 mmol/l. Repeated infusions of 200-300 ml hypertonic 3% sodium chloride solution, gluco- and mineralocorticoid therapy was ineffective, increasing plasma sodium levels by 2-3 mmol/l with the return to the initial level during 6-8 hours. Hypopituitary disorders did not develop after surgery. With further observation, the sodium level remained within 126-129 mmol/l for 6 months after surgery. The water load test make exclude the classic syndrome of inappropriate secretion of antidiuretic hormone, and confirmed the diagnosis of RSO. Because of absence of clinical symptoms associated with hyponatremia, no medical correction was required, patient was recommended to clinical follow-up.

Hydrogen sulfide (H2S), an endogenous signaling molecule, is known to play a pivotal role in neuroprotection, vasodilation, and hormonal regulation. To further explore the biological effects of H2S, refined donors that facilitate its biological delivery, especially under specific (patho) physiological conditions, are needed. In the present study, we demonstrate that ortho-substituted, aryl boronate esters provide two unique and distinct pathways for H2S release from thioamide-based donors: Lewis acid-facilitated hydrolysis and reactive oxygen species (ROS)-induced oxidation/cyclization. Through a detailed structure-activity relationship study, donors that resist hydrolysis and release H2S solely via the latter mechanism were identified, which have the added benefit of providing a potentially useful heterocycle as the lone byproduct of this novel chemistry. To highlight this, we developed an ROS-activated donor (QH642) that simultaneously synthesizes a benzoxazole-based fluorophore en route to its H2S delivery. A distinct advantage of this design over earlier self-reporting donors is that fluorophore formation is possible only if H2S has been discharged from the donor. This key feature eliminates the potential for false positives and provides a more accurate depiction of reaction progress and donor delivery of H2S, including in complex cellular environments.

Applied pesticides end up in non-target environments as complex mixtures. When bioavailable, these chemicals pose a threat to living organisms and can induce oxidative stress (OS). In this article, attention is paid to OS and the physiological role of the antioxidant defense system. South African and international literature was reviewed to provide extensive evidence of pesticide-induced OS in non-target organisms, in vivo and in vitro. Although in vitro approaches are used internationally, South African studies have only used in vivo methods. Considering ethical implications, the authors support the use of in vitro bioassays to screen environmental matrices for their OS potential. Since OS responses are initiated and measurable at lower cellular concentrations compared to other toxicity endpoints, in vitro OS bioassays could be used as an early warning sign for the presence of chemical mixtures in non-target environments. Areas of concern in the country could be identified and prioritized without using animal models. The authors conclude that it will be worthwhile for South Africa to include in vitro OS bioassays as part of a battery of tests to screen environmental matrices for biological effects. This will facilitate the development and implementation of biomonitoring programs to safeguard the South African environment.

Stroke, the second leading cause of death worldwide, is a complex disease influenced by many risk factors among which we can find reactive oxygen species (ROS). Since mitochondria are the main producers of cellular ROS, nowadays studies are trying to elucidate the role of these organelles and its DNA (mtDNA) variation in stroke risk. The aim of the present study was to perform a comprehensive evaluation of the association between mtDNA mutations and mtDNA content and stroke risk.
Homoplasmic and heteroplasmic mutations of the mtDNA were analysed in a case-controls study using 110 S cases and their corresponding control individuals. Mitochondrial DNA copy number (mtDNA-CN) was analysed in 73 of those case-control pairs.
Our results suggest that haplogroup V, specifically variants m.72C > T, m.4580G > A, m.15904C > T and m.16298 T > C have a protective role in relation to stroke risk. On the contrary, variants m.73A > G, m.11719G > A and m.14766C > T appear to be genetic risk factors for stroke. In this study, we found no statistically significant association between stroke risk and mitochondrial DNA copy number.
These results demonstrate the possible role of mtDNA genetics on the pathogenesis of stroke, probably through alterations in mitochondrial ROS production.