COVID-19, caused by SARS-CoV-2, is characterized by pneumonia, lymphopenia, exhausted lymphocytes and a cytokine storm. Several reports from around the world have identified obesity and severe obesity as one of the strongest risk factors for COVID-19 hospitalization and mechanical ventilation. Moreover, countries with greater obesity prevalence have a higher morbidity and mortality risk of developing serious outcomes from COVID-19. The understanding of how this increased susceptibility of the people with obesity to develop severe forms of the SARS-CoV-2 infection occurs is crucial for implementing appropriate public health and therapeutic strategies to avoid COVID-19 severe symptoms and complications in people living with obesity. We hypothesize here that increased ACE2 expression in adipose tissue displayed by people with obesity may increase SARS-CoV-2 infection and accessibility to this tissue. Individuals with obesity have increased white adipose tissue, which may act as a reservoir for a more extensive viral spread with increased shedding, immune activation and pro-inflammatory cytokine amplification. Here we discuss how obesity is related to a pro-inflammatory and metabolic dysregulation, increased SARS-CoV-2 host cell entry in adipose tissue and induction of hypercoagulopathy, leading people with obesity to develop severe forms of COVID-19 and also death. Taken together, it may be crucial to better explore the role of visceral adipose tissue in the inflammatory response to SARS-CoV-2 infection and investigate the potential therapeutic effect of using specific target anti-inflammatories (canakinumab or anakinra for IL-1β inhibition; anti-IL-6 antibodies for IL-6 inhibition), anticoagulant or anti-diabetic drugs in COVID-19 treatment of people with obesity. Defining the immunopathological changes in COVID-19 patients with obesity can provide prominent targets for drug discovery and clinical management improvement.

Zika virus (ZIKV) has a strong tropism for the nervous system and has been related to post-infection neurological syndromes. Once neuronal cells are infected, the virus is capable of modulating cell metabolism, leading to neurotoxicity and cellular death. The negative effect of ZIKV in neuron cells has been characterized. However, the description of molecules capable of reversing these cytotoxic effects is still under investigation. In this context, it has been largely demonstrated that docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid, is highly neuroprotective. Here, we hypothesized that DHA’s neuroprotective proprieties could have an influence on ZIKV-induced neurotoxicity in SH-SY5Y cells. Our data showed that pre-treatment of SH-SY5Y cells with DHA increased the cell viability and proliferation in ZIKV-infected cells. Moreover, DHA triggered an anti-inflammatory response in those infected cells. Besides, DHA was capable of restoring mitochondria function and number in ZIKV-infected SH-SY5Y cells. In addition, cells pre-treated with DHA prior to ZIKV infection presented a lower viral load at different times of infection. Taking together, these results demonstrated that DHA has a potential anti-inflammatory and neuroprotective effect against ZIKV infection in these neuron-like cells and could be a useful tool in the treatment against this virus.

The present study reports the synthesis and crystal structure of four novel gold(I) complexes with di-2-pyridyl ketone N(4)-ethylthiosemicarbazone (L¹) and 2-acetylfuran-4-methyl-3-thiosemicarbazone (L²). All the gold(I) complexes were observed with monodentate thiosemicarbazones and exhibited gold(I) ions with linear geometries, bound to a sulfur atom of the ligand and a halogen ion (Br⁻ or Cl⁻). The crystal structures of gold complexes with Br⁻ and thiosemicarbazone are the first examples reported. Interestingly, 2[AuBr(HL¹)]2Br was observed to have a Au⋯Au length of 3.155(8) Å, and this distance suggests an unusual Au⋯Au interaction in the solid state. The ability of the thiosemicarbazones and the corresponding gold(I) complexes to bind to DNA was studied by UV-vis and emission spectroscopy. The effect on cell viability of the compounds was evaluated against human breast cancer cell lines. The results show that the gold(I) complexes exhibit more potent inhibition of tumor growth than the free ligands.

Liver cancer is one of the most lethal malignancies and is commonly diagnosed as hepatocellular carcinoma (HCC), a tumor type that affects about 90% of patients. Non-alcoholic steatohepatitis (NASH) and obesity are both risk factors for this disease. HCC initiation and progression are deeply linked with changes in the hepatic microenvironment, with cytokines playing key roles. The understanding of the pathogenic pathways that connect these disorders to liver cancer remains poor. However, the inflammasome-mediated cytokines associated with both diseases are central actors in liver cancer progression. The release of the pro-inflammatory cytokines IL-1β and IL-18 during inflammasome activation leads to several detrimental effects on the liver microenvironment. Considering the critical crosstalk between obesity, NASH, and HCC, this review will present the connections of IL-1β and IL-18 from obesity-associated NASH with HCC and will discuss approaches to using these cytokines as therapeutic targets against HCC.

Background/Objectives: In recent years, silver nanoparticles (AgNPs) have garnered significant attention due to their potent antimicrobial properties, which hold promise for various applications. However, concerns about their potential toxicity have also emerged, particularly regarding their impact on human and animal health. This study investigates the acute toxicological effects of AgNPs synthesized using a green route with an aqueous extract of a native Cerrado plant (AgNPs-Cb) in mice. Methods: The AgNPs-Cb were intravenously administered at a concentration of 64 µM, and the mice were euthanized after 24 h for the collection of blood and organ samples (liver, spleen, kidneys, and lungs) for hematological, biochemical, and histological analyses. Results: Hematological analysis, including complete blood count (CBC) and differential leukocyte count, showed no statistically significant alterations in the groups treated with AgNPs-Cb, Cb extract, and Ag⁺, compared with the control group (p < 0.05). Notably, only the Ag⁺ group exhibited a significant increase in red blood cell count and hematocrit levels, suggesting that the nanoformulation of silver might mitigate the hematological impact seen with free silver ions. Biochemical analyses of liver and kidney function markers also revealed no significant differences across the treatment groups. Conclusions: These findings indicate that AgNPs-Cb may offer a safer alternative for antimicrobial applications, reducing the risk of acute toxicity in mammals while maintaining efficacy against pathogens. Further studies are needed to explore the underlying mechanisms and long-term effects of AgNPs-Cb exposure.

Ovarian cancer remains one of the most lethal gynecologic malignancies due to late diagnosis, limited treatment options, and frequent chemoresistance. Docosahexaenoic acid (DHA), a long-chain omega-3 polyunsaturated fatty acid, has been associated with anti-tumor effects in various cancer models. Here, we investigated the effects of DHA on cell death, oxidative stress, and mitochondrial function in A2780 human ovarian cancer cells. Our data show that DHA decreases cell viability and proliferation in a dose- and time-dependent manner, promoting lytic cell death with increased membrane permeability and LDH release. We identified pyroptosis as the predominant death mechanism, evidenced by caspase-1 activation, pore formation, and mitochondrial dysfunction. DHA treatment rapidly increased intracellular reactive oxygen species (ROS) and mitochondrial superoxide levels, which were essential for both membrane pore formation and the loss of mitochondrial membrane potential. Notably, ROS scavenging with N-acetylcysteine reversed DHA-induced mitochondrial damage and pyroptosis, indicating ROS dependence. Furthermore, DHA reduced mitochondrial content and impaired spare respiratory capacity, suggesting disrupted mitochondrial adaptability. Caspase-1 inhibition restored both mitochondrial integrity and respiratory function, highlighting a mechanistic role for caspase-1 in mediating DHA-induced bioenergetic dysfunction. Collectively, our findings reveal that DHA compromises ovarian cancer cell survival by triggering ROS- and caspase-1-dependent pyroptosis and mitochondrial dysfunction. This study expands the understanding of DHA’s anti-cancer mechanisms and positions it as a promising candidate for adjuvant therapies targeting mitochondrial vulnerabilities and immunogenic cell death pathways in ovarian cancer.