Arsenic is a widespread environmental metalloid whose inorganic forms contaminate drinking water, food chains, soil and air. Male reproductive toxicity is biologically plausible because spermatogenesis, steroidogenesis and post-testicular sperm maturation depend on tightly regulated redox, metabolic and endocrine processes. Yet the evidential basis for attributing human male subfertility to environmental arsenic remains markedly less secure than the experimental literature might suggest. This critical narrative review integrates exposure science, human epidemiology, animal and cell-model evidence, mechanistic research and methodological limitations. Literature published from 1980 to 1 June 2026 was identified through PubMed/MEDLINE, authoritative institutional websites and supplementary scholarly web searching, with backward and forward citation checking. Human studies provide signals of lower sperm concentration or motility, altered seminal biomarkers, infertility-associated urinary arsenic species and perturbation of steroid-hormone excretion. These findings are not uniform: studies are few, often clinic-based and cross-sectional, and differ in arsenic speciation, exposure range, co-exposures, semen assessment and confounder control. Experimental evidence is more coherent, linking arsenite and related compounds to oxidative injury, mitochondrial dysfunction, germ-cell loss, impaired spermatid elongation, acrosomal and flagellar defects, epididymal dysfunction, endocrine disruption, autophagy and altered sperm proteins. Developmental exposure and incomplete recovery after withdrawal raise concern about vulnerable windows, although doses and species frequently limit direct translation to human environmental exposure. The strongest current inference is that arsenic can damage male reproductive biology and may contribute to impaired semen quality in susceptible or highly exposed populations; the magnitude of risk at common low-level exposure is uncertain. Progress requires prospective preconception cohorts, repeated arsenic speciation and semen sampling, mixture-aware analysis, functional sperm and fertility outcomes, and explicit evaluation of reversibility after exposure reduction. Prevention should prioritise exposure control rather than unvalidated arsenic-specific fertility treatments.
S. K. Nayak, B. Behra, Mohammed Shoeb et al.· Asian Journal of Biology· 0 citations
Myostatin b (mstnb), a key negative regulator of skeletal muscle growth, represents a promising target gene for genome editing aimed at enhancing growth performance and aquaculture productivity. The present study aimed to design, construct and in silico validate a donor DNA carrying a single-nucleotide substitution that introduces a premature stop codon in the mstnb gene of Labeo rohita for RNA-guided recombinase (RGR) platform-mediated genome editing. For this purpose the mstnb gene sequence was retrieved from the NCBI database and analysed to identify an appropriate target site within exon 1. A targeted single nucleotide substitution from guanine to thymine (G > T) was strategically planned into the donor DNA upstream of the native stop codon to convert the glycine codon (GGA) into a premature stop codon (TGA). This was achieved by identifying RGR target sites flanking the intended mutation site and designing specific primers to amplify and clone the DNA fragment. The target 600 bp DNA fragment encompassing the mutation site flanked by two RGR target sites was successfully amplified and ligated into the pJET1.2 cloning vector and confirmed through Sanger sequencing. Site-directed mutagenesis successfully introduced the intended nucleotide substitution, which was subsequently confirmed by Sanger sequencing. Computational analyses using InterPro, ColabFold, SWISS-MODEL and CYS_REC predicted that the introduced nonsense mutation would generate a truncated Mstnb protein, resulting in the loss of conserved TGF-β domains, reduced structural stability, and impaired cytokine activity. Structural modelling further revealed disruption of the C-terminal β-sheet structure, reduced stereochemical quality, altered QMEAN Z-scores, and loss of cysteine residues, collectively indicating impaired protein folding and reduced structural stability. These findings suggest that the engineered mutation is likely to abolish the functional activity of the mstnb gene, thereby providing a validated donor DNA construct for precise RGR-mediated genome editing in L. rohita. Future studies will focus on the experimental validation of the engineered donor DNA construct through RGR-mediated genome editing, followed by functional characterization in L. rohita.