Magnesium oxide is typically white and can be colorized with transition metal insertion by doping. We present the preparation of a green-colored hydroxide by the exchange of Mg2+ on the crystalline lattice with Ni2+ in MgO, using three nickel salts. MgOst was prepared by the colloidal starch suspension method, using cassava starch. The oxides and hydroxides, before and after, were characterized by X-ray diffraction (XRD), and show that a phase change occurs: a transition from periclase (MgO) to brucite (Mg(OH)2) due to the incorporation of nickel ions from different salts (acetate, chloride, and nitrate), resulting in the solid solution [NixMg1−x(OH)2]. The FTIR spectrum corroborates the crystallographic structure identified through XRD patterns, confirming the formation of a crystal structure resembling brucite. The new samples present a green color, indicative of the incorporation of the Ni2+ ions. The antimicrobial activity of products resulting from the doping of magnesium oxide with nickel and the precursor MgOst was assessed through the minimum inhibitory concentration (MIC) test. The evaluation included three bacterial strains: Staphylococcus aureus (ATCC 25923), Escherichia coli (ATCC 25922), Salmonella gallinarum (ATCC 9184), and a yeast strain, Candida albicans (ATCC 10231). The obtained results were promising; the tested samples exhibited antimicrobial activity, with a MIC ranging from 0.312 to 0.625 μg.μL−1. The nickel compound, derived from the precursor chloride salt, demonstrated superior MIC activity. Notably, all tested samples displayed bactericidal activity against the S. aureus strain and exhibited a broad spectrum of inhibition, encompassing both Gram-positive and Gram-negative strains. Only the nickel compounds derived from precursors with acetate and nitrate anions demonstrated antimicrobial activity against C. albicans, exhibiting a fungistatic behavior. Based on the conducted studies, [NixMg1−x(OH)2] has emerged as a promising antimicrobial agent, suitable for applications requiring the delay or inhibition of bacterial growth.