Arsenic (As) and cadmium (Cd) are elements arousing major public health concerns associated with environmental pollution, high toxicity potential, and carcinogenic nature. However, selenium (Se) at low doses and incorporated into enzymes and proteins has antioxidant properties and protects animals and humans from the risk of various diseases. It also has an exceptionally narrow range between necessary and toxic concentrations, which is a well-known hindrance in its use as a dietary supplement. The present article aims to update and expand the role of Se in As and Cd toxicity discussed in our earlier paper. In general, recent reports show that Se, regardless of its form (as selenite, selenomethionine, nanoSe, or Se from lentils), can reduce As- or Cd-mediated toxicity in the liver, kidney, spleen, brain, or heart in animal models and in cell culture studies. As was suggested in our earlier review, Se antagonizes the toxicity of As and Cd mainly through sequestration of these elements into biologically inert complexes and/or through the action of Se-dependent antioxidant enzymes. An increase in the As methylation efficiency is proposed as a possible mechanism by which Se can reduce As toxicity. However, new studies indicate that Se may also diminish As or Cd toxicity by activation of the Nrf2 pathway. In addition, this paper discusses possible signs of Se toxic effects, which may be a challenge for its future use in the therapy of As and Cd poisoning and provide future directions to address this issue.

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The Role of Selenium in Arsenic and Cadmium Toxicity: an Updated Review of Scientific Literature

H2S belongs to the class of molecules known as gasotransmitters, which also includes nitric oxide (NO) and carbon monoxide (CO). Three enzymes are recognized as endogenous sources of H2S in various cells and tissues: cystathionine g-lyase (CSE), cystathionine β-synthase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST). The current article reviews the regulation of these enzymes as well as the pathways of their enzymatic and non-enzymatic degradation and elimination. The multiple interactions of H2S with other labile endogenous molecules (e.g. NO) and reactive oxygen species are also outlined. The various biological targets and signaling pathways are discussed, with special reference to H2S and oxidative posttranscriptional modification of proteins, the effect of H2S on channels and intracellular second messenger pathways, the regulation of gene transcription and translation and the regulation of cellular bioenergetics and metabolism. The pharmacological and molecular tools currently available to study H2S physiology are also reviewed, including their utility and limitations. In subsequent sections, the role of H2S in the regulation of various physiological and cellular functions is reviewed. The physiological role of H2S in various cell types and organ systems are overviewed. Finally, the role of H2S in the regulation of various organ functions is discussed as well as the characteristic bell-shaped biphasic effects of H2S. In addition, key pathophysiological aspects, debated areas, and future research and translational areas are identified A wide array of significant roles of H2S in the physiological regulation of all organ functions emerges from this review.

Physiological roles of hydrogen sulfide in mammalian cells, tissues and organs.

The antagonistic effect of selenium on cadmium-induced apoptosis via PPAR-γ/PI3K/Akt pathway in chicken pancreas.

Puerarin reverses cadmium-induced lysosomal dysfunction in primary rat proximal tubular cells via inhibiting Nrf2 pathway

Oxidative stress-induced skeletal muscle injury involves in NF-κB/p53-activated immunosuppression and apoptosis response in copper (II) or/and arsenite-exposed chicken.

Cadmium induces BNIP3-dependent autophagy in chicken spleen by modulating miR-33-AMPK axis.

Cadmium-mediated miR-30a-GRP78 leads to JNK-dependent autophagy in chicken kidney.

. In this paper, we give some characterizations of h -convex functions, and some appli- cations related to these functions are also obtained. According to these results, we can know better the relation between convex functions and h -convex functions.

Some characterizations of h-convex functions

. In this paper, we present an inequality of matrix norms, which is a generalization of the inequality shown by Zou [Linear Algebra Appl. 562, 154–162].

A matrix inequality for unitarily invariant norms

We prove homological mirror symmetry for the universal centralizer JG, associated with any complex reductive Lie groupG. This is a continuation of the author’s previous work [Jin1] on proving the result for G of adjoint form.

Homological mirror symmetry for the universal centralizers ii: the general case and induction pattern

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