Interplay between Estrogen, Kynurenine, and AHR Pathways: An immunosuppressive axis with therapeutic potential for breast cancer treatment.

Breast cancer is one of the most common malignancies among women worldwide. Estrogen exposure via endogenous and exogenous sources during a lifetime, together with environmental exposure to estrogenic compounds, represent the most significant risk factor for breast cancer development. As breast tumors establish, multiple pathways are deregulated.

Cobalt protoporphyrin decreases food intake, body weight, and the number of neurons in the Nucleus Accumbens in female rats.

Cobalt protoporphyrin (CoPP) is a potent heme oxygenase-1 inductor that produces temporary hypophagia and chronic weight loss. A complete description of this effect and the underlying mechanisms are unknown. In this work, we challenged the ability of CoPP to produce changes in rat behavior and cellular alterations in the Nucleus Accumbens that would explain those effects.

Astrocytes Are More Vulnerable than Neurons to Silicon Dioxide Nanoparticle Toxicity in Vitro.

Some studies have shown that silicon dioxide nanoparticles (SiO-NPs) can reach different regions of the brain and cause toxicity; however, the consequences of SiO-NPs exposure on the diverse brain cell lineages is limited. We aimed to investigate the neurotoxic effects of SiO-NP (0-100 µg/mL) on rat astrocyte-rich cultures or neuron-rich cultures using scanning electron microscopy, Attenuated Total Reflection-Fourier Transform Infrared spectroscopy (ATR-FTIR), FTIR microspectroscopy mapping (IQ mapping), and cell viability tests. SiO-NPs were amorphous particles and aggregated in saline and culture media.

Sulforaphane prevents quinolinic acid-induced mitochondrial dysfunction in rat striatum.

Quinolinic acid (QA) triggers striatal neuronal death by an excitotoxic cascade that involves oxidative stress, which in turns is tightly linked to mitochondria. Mitochondrial dysfunction is a molecular feature described in several brain pathologies. In this work, we determined whether the sulforaphane-neuroprotective effect in the rodent experimental model of Huntington's disease induced by QA is associated with mitochondrial function preservation.

Chronic exposure to low levels of inorganic arsenic causes alterations in locomotor activity and in the expression of dopaminergic and antioxidant systems in the albino rat.

Several studies have associated chronic arsenicism with decreases in IQ and sensory and motor alterations in humans. Likewise, studies of rodents exposed to inorganic arsenic ((i)As) have found changes in locomotor activity, brain neurochemistry, behavioral tasks, oxidative stress, and in sensory and motor nerves. In the current study, male Sprague-Dawley rats were exposed to environmentally relevant doses of (i)As (0.