Seaweed biochar is an efficient alternative bioadsorbent for Cu²⁺ removal due to its low cost and heavy metal removal capacity. Using the slow pyrolysis process, we produced biochars from Macrocystis pyrifera at 300 (BC300), 450 (BC450), and 600 °C (BC600). The physicochemical and structural properties of the biochar samples improved with increasing pyrolysis temperature from 300 to 450 °C, whereas no significant differences were observed with further increases in temperature to 600 °C. The yield ranged between 49% and 62% and had a high ash content (57.5–71.1%). BC450 and BC600 presented the highest surface areas and higher porosities. The FTIR spectra indicated that an increase of temperature decreased the acidic functional groups due to depolymerization and the dehydration processes, increasing the aromatic structures and the presence of calcium carbonate. The fittings of the kinetic models were different for the BCs: for the BC450 and BC600 samples, the Cu²⁺ adsorption was well-represented by a pseudo-first-order model; for BC300, a better fit was obtained with the pseudo-second-order model. The rate-limiting step of Cu²⁺ adsorption on BCs was represented by both models, liquid film diffusion and intraparticle diffusion, with surface diffusion being more important in BC300 and BC600, and intraparticle diffusion in BC450, in agreement with the pore size of the biochar samples. The adsorption isotherms of all BCs showed Langmuir behavior, representative of a chemisorption process, which was corroborated by the energy adsorption values determined by the D–R model. The maximum monolayer Cu²⁺ adsorption capacities were 93.55 and 58.0 mg g⁻¹ for BC600 and BC450, respectively, whereas BC450 presented the highest affinity. Other mechanisms involved in controlling heavy metal removal from aqueous suspensions using these seaweed biochars remain to be explored. We conclude that BC450 and BC600 from M. pyrifera are the most efficient adsorbents for Cu²⁺ aqueous removal and are thus an appropriate alternative for bioremediation.

Aging is a significant risk factor for male fertility and can lead to severe developmental disorders in offspring. It disrupts testicular function and spermatogenesis, resulting in sperm abnormalities and DNA fragmentation. Male aging alters the genome and epigenome of germ cells due to persistent oxidative stress caused by the cumulative effects of environmental factors over a lifetime. At the molecular level, DNA damage occurs and is poorly repaired due to impaired DNA repair pathways, leading to unrepaired lesions and de novo mutations. Aging also creates distinct epigenetic landscapes that modify gene expression in germ cells, affect the DNA damage response, and generate de novo DNA and epigenetic mutations that are transmitted to the sperm and inherited by the offspring. This review discusses current knowledge on the age-associated effects on male germ cells and the genomic and epigenomic mechanisms contributing to altered male reproductive health and outcomes in progeny. We propose a male reproductive aging threshold, where cumulative exposure to risk factors leads to oxidative stress, impaired spermatogenesis, and altered reproductive outcomes. Finally, we discuss novel interventions to prevent premature testicular aging and emphasize the need for public health policies and counseling guidelines for men seeking paternity.