Lead (Pb) has been used by humans since prehistoric times to make tools due to its malleability and durability. The Roman Empire, the Industrial Revolution, and the introduction of Pb in gasoline during the 1920s contributed to increased environmental concentrations. Pb toxicity led to its removal from gasoline after several decades. However, Pb continues to be emitted from various anthropogenic sources, including but not limited to batteries, mining, foundries, smelting, e-waste recycling, and painting. Pb remains an environmental concern, as no established safe concentration for human health has been identified. Children are more susceptible to the absorption and poisoning of Pb. Occupational exposure to Pb poses a significant risk to workers and individuals living near lead industries. The primary routes of exposure are inhalation and ingestion, and bioaccumulation and biomagnification through the food chain are major sources of human exposure. This review aims to provide an overview of Pb and its systemic toxicity of Pb, including its effects on the lungs, blood, liver, kidneys, and nervous, cardiovascular, and reproductive systems. Since Pb is classified as a probable carcinogen for humans, the article also addresses genotoxicity and cancer risk. Furthermore, it reviews the most researched mechanisms of toxicity, including calcium mimicry, oxidative stress, and inflammation, along with other less-studied mechanisms. Nevertheless, the authors emphasize the importance of exploring less examined cells, tissues, and mechanisms to deepen the understanding of Pb toxicity at various concentrations, particularly in cases of chronic low-level Pb exposure, to develop better prevention and treatment strategies for lead poisoning.

Particulate atmospheric pollution poses a global threat to human health. Metals enter the body through inhalation attached to these particles. Certain vulnerable groups are more susceptible to toxicity because of age, physiological changes, and chronic and metabolic diseases and also workers because of high and cumulative exposure to metals. A narrative review was conducted to examine the effects of key metals—arsenic, cadmium, chromium, copper, lead, mercury, manganese, nickel, vanadium, and zinc—on vulnerable populations, analyzing articles published over the past decade. Some of these metals are essential for humans; however, excessive levels are toxic. Other non-essential metals are highly toxic. Shared mechanisms of toxicity include competing with other minerals, oxidative stress and inflammation, and interacting with proteins and enzymes. Prenatal and childhood exposures are particularly concerning because they can interfere with neurodevelopment and have been associated with epigenetic changes that have long-term effects. Occupational exposure has been studied, but current exposure limits for specific metals appear dangerous, emphasizing the need to revise these standards. Older adults, pregnant women, and individuals with metabolic diseases are among the least studied groups in this review, underscoring the need for more research to understand these populations better and create effective public health policies.

In this century, cancer is one of the most important causes of death worldwide, and the need for the development of new treatment options is imperative. The use of metal-based compounds in cancer treatment has increased significantly due to certain properties of these elements, and vanadium has been one of the most studied transition metals in recent decades. Vanadium compounds are being explored as an option for cancer treatment because of their wide range of action mechanisms such as the induction of oxidative stress, DNA damage, cell cycle arrest, induction of apoptosis and regulation of the autophagy process, among the most important mechanisms. Their compounds have been demonstrated to be effective against the cancer types with the highest incidence and mortality rates worldwide, such as lung and breast cancer, with promising results. This review discusses a variety of new vanadium compounds, indicating their mechanisms of action and the neoplasms in which they have shown effectiveness.

• Oral administration of sodium metavanadate 10 mg/kg decreased parasitemia and increased survival in the Pyy mice model. • Oral administration of 10 mg/kg of sodium metavanadate was neither genotoxic nor cytotoxic in the Pyy mice model. • Sodium metavanadate is proposed as a potential antimalaric agent.

Apicomplexan parasites are the causal agents of different medically important diseases, such as toxoplasmosis, cryptosporidiosis, and malaria. Toxoplasmosis is considered a neglected parasitosis, even though it can cause severe cerebral complications and death in immunocompromised patients, including children and pregnant women. Drugs against Toxoplasma gondii, the etiological agent of toxoplasmosis, are highly toxic and lack efficacy in eradicating tissue cysts, promoting the establishment of latent infection and acute relapsing disease. Cryptosporidiosis has been recognized as the most frequent waterborne parasitosis in US outbreaks; anti-cryptosporidium drug discovery still faces a major obstacle: drugs that can act on the epicellular parasite. Severe malaria is most commonly caused by the progression of infection with Plasmodium falciparum. In recent years, great progress has been made in the field of antimalarial drugs and vaccines, although the resistance of P. falciparum to artemisinin has recently gained a foothold in Africa. As seen, the search for new drugs against these parasites remains a challenge. Peptide-based drugs seem to be attractive alternative therapeutic agents recently recognized by the pharmaceutical industry, as they can kill different infectious agents and modulate the immune response. A review of the experimental effects of bioactive peptides on these parasites follows, along with comments. In addition, some biological and metabolomic generalities of the parasites are reviewed to elucidate peptide mechanisms of action on Apicomplexan targets.

Revista de la Facultad de Medicina de la UNAM