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Formaldehyde is ubiquitous pollutant that induces oxidative stress in the lung. Several lung diseases have been associated with oxidative stress and their control is necessary. Photobiomodulation therapy (PBMT) has been highlighted as a promissory treatment, but its mechanisms need to be better investigated. Our objective was to evaluate the effects of PBMT on the oxidative stress generated by FA exposure. Male Wistar rats were submitted to FA exposure of 1% or vehicle (3 days) and treated or not with PBMT (1 and 5 h after each FA exposure). Rats treated only with laser were used as control. Twenty-four hours after the last FA exposure, we analyzed the effects of PBMT on the generation of nitrites and hydrogen peroxide, oxidative burst, glutathione reductase, peroxidase, S-transferase enzyme activities, the gene expression of nitric oxide, cyclooxygenase, superoxide dismutase, the catalase enzyme, and heme oxygenase-1. PBMT reduced the generation of nitrites and hydrogen peroxide and increased oxidative burst in the lung cells. A decreased level of oxidant enzymes was observed which were concomitantly related to an increased level of antioxidants. This study provides new information about the antioxidant mechanisms of PBMT in the lung and might constitute an important tool for lung disease treatment.

Despite scientific evidence and government actions aimed at reducing air pollution, it remains a major public health issue in large urban centers, compromising human health, particularly among the most vulnerable populations, including the elderly. Polyphenolic compounds are believed to have antiaging effects, reducing DNA damage and exhibiting anti‐inflammatory and antioxidant properties. The polyphenol resveratrol (Resv) has demonstrated protective effects in the lungs against harmful stimuli in adult mice; however, few studies have extended these investigations to elderly animals, which have reduced antioxidant responses. This study aimed to evaluate the effects of Resv on the lungs of 15‐month‐old mice exposed to diesel exhaust (DE). Animals were exposed to 1200 µg/m3 of PM2.5 over 30 consecutive days. Resv (1200 µg/m3) was administered for 40 days, beginning 10 days before DE exposure. We evaluated the inflammatory profile in bronchoalveolar lavage fluid (BALF) and serum; quantified macrophages; and assessed antioxidant enzymes (glutathione peroxidase [GPx], glutathione reductase [GR], glutathione‐S‐transferase [GST], and copper/zinc superoxide dismutase [Cu/Zn SOD]), 8‐OHdG, 8‐iso‐prostaglandin F2α (8‐isoprostane), collagen and elastic fiber content, and sirtuin protein levels (Sirt1, Sirt2, and Sirt6) in the lung parenchyma. Resv administration increased GR and Sirt1 levels and decreased Sirt2 levels. DE caused inflammatory changes in BALF and lung tissue, increased 8‐OHdG and 8‐isoprostane levels, and modulated antioxidant enzymes, sirtuins, and lung collagen. Resv administration after DE exposure did not significantly alter 8‐OHdG, antioxidant enzymes, sirtuins, or collagen levels in the lungs, but it reduced BALF cellularity and IL‐1β and 8‐isoprostane levels. Our data suggest moderate protective effects of Resv in aged lungs exposed to DE.

Crack cocaine users are simultaneously exposed to volatilized cocaine and to its main pyrolysis product, anhydroecgonine methyl ester (AEME). Although the neurotoxic effects of cocaine have been extensively studied, little is known about AEME or its combination. We investigated cell death processes using rat primary hippocampal cells exposed to cocaine (2 mM), AEME (1 mM) and their combination (C + A), after 1, 3, 6 and 12 h. Cocaine increased LC3 I after 6 h and LC3 II after 12 h, but reduced the percentage of cells with acid vesicles, suggesting failure in the autophagic flux, which activated the extrinsic apoptotic pathway after 12 h. AEME neurotoxicity did not involve the autophagic process; rather, it activated caspase-9 after 6 h and caspase-8 after 12 h leading to a high percentage of cells in early apoptosis. C + A progressively reduced the percentage of undamaged cells, starting after 3 h; it activated both apoptotic pathways after 6 h, and was more neurotoxic than cocaine and AEME alone. Also, C + A increased the phosphorylation of p62 after 12 h, but there was little difference in LC3 I or II, and a small percentage of cells with acid vesicles at all time points investigated. In summary, the present study provides new evidence for the neurotoxic mechanism and timing response of each substance alone and in combination, indicating that AEME is more than just a biological marker for crack cocaine consumption, as it may intensify and hasten cocaine neurotoxicity.