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Looking for the LOAEL or NOAEL Concentration of Nickel-Oxide Nanoparticles in a Long-Term Inhalation Exposure of Rats.

ABSTRACT: Rats were exposed to nickel oxide nano-aerosol at a concentration of 2.4 ± 0.4 µg/m³ in a "nose only" inhalation setup for 4 h at a time, 5 times a week, during an overall period of 2 weeks to 6 months. Based on the majority of the effects assessed, this kind of exposure may be considered as close to LOAEL (lowest observed adverse effect level), or even to NOAEL (no observed adverse effect level). At the same time, the experiment revealed genotoxic and allergic effects as early as in the first weeks of exposure, suggesting that these effects may have no threshold at all.

SUBMITTER: Katsnelson BA

PROVIDER: S-EPMC7796390 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Looking for the LOAEL or NOAEL Concentration of Nickel-Oxide Nanoparticles in a Long-Term Inhalation Exposure of Rats.

Katsnelson Boris A BA Chernyshov Ivan N IN Solovyeva Svetlana N SN Minigalieva Ilzira A IA Gurvich Vladimir B VB Valamina Irene E IE Makeyev Oleg H OH Sahautdinova Renata R RR Privalova Larisa I LI Tsaregorodtseva Anastasia E AE Korotkov Artem V AV Shuman Eugene A EA Panov Vladimir G VG Sutunkova Marina P MP

International journal of molecular sciences 20210103 1

Rats were exposed to nickel oxide nano-aerosol at a concentration of 2.4 ± 0.4 µg/m<sup>3</sup> in a "nose only" inhalation setup for 4 h at a time, 5 times a week, during an overall period of 2 weeks to 6 months. Based on the majority of the effects assessed, this kind of exposure may be considered as close to LOAEL (lowest observed adverse effect level), or even to NOAEL (no observed adverse effect level). At the same time, the experiment revealed genotoxic and allergic effects as early as in ...[more]

PMID: 33401533

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Project description:Copper oxide nanoparticles (CuO NPs) are considered for various technological and consumer applications, leading to growing concerns for potential human hazards resulting from inhalation. Recent studies have revealed a dose-dependent toxicity of CuO NPs in rats following short-term inhalation exposure. Here, we utilized transcriptomics approaches to further investigate the responses in rats exposed via inhalation for five consecutive days to two doses of CuO NPs, 3.3 (low dose, LD) and 13.2 (high dose, HD) mg/m3, with collection of lung tissues on days 6 (1 day post-exposure) and 28 (i.e., after a 22-day post-exposure recovery period). Histopathology confirmed an acute inflammatory response that was resolved during the post-exposure phase. Global gene expression analyses yielded about 1,000 differentially expressed genes in HD rats and 200 in LD on day 6, and less than 20 after the recovery period. Pathway analysis indicated cell proliferation/survival and inflammation as the main processes triggered by exposure and identified epithelial cell transforming protein 2 (Ect2) as a potential gene of interest implicated in cell proliferation. Indeed, ECT2 was upregulated in exposed lungs and was localized in the cytoplasm of alveolar epithelial cells in HD rats, in hyperplasic foci identified based on the Ki67 antigen, a marker of cell proliferation. Monocyte chemoattractant protein 1 (MCP-1, also known as CCL2), with an important role in the regulation of inflammatory processes and cell proliferation, was also upregulated and this was confirmed immunohistochemically. Finally, we could not find any evidence for aberrant DNA methylation of inflammation-associated genes in response to CuO NP exposure. In summary, the current findings suggest that airborne CuO NPs cause an acute response that translates into inflammation and cellular proliferation in bronchoalveolar epithelium, with upregulation of neoplasia-related factors even after a short-term exposure.

Project description:BackgroundInhalation exposure to nanomaterials in workplaces can include a mixture of multiple nanoparticles. Such ambient nanoparticles can be of high dissolution or low dissolution in vivo and we wished to determine whether co-exposure to particles with different dissolution rates affects their biokinetics.Methods and resultsRats were exposed to biosoluble silver nanoparticles (AgNPs, 10.86 nm) and to biopersistent gold nanoparticles (AuNPs, 10.82 nm) for 28 days (6-h/day, 5-days/week for 4 weeks) either with separate NP inhalation exposures or with combined co-exposure. The separate NPs mass concentrations estimated by the differential mobility analyzer system (DMAS) were determined to be 17.68 ± 1.69 μg/m3 for AuNP and 10.12 ± 0.71 μg/m3 for AgNP. In addition, mass concentrations analyzed by atomic absorption spectrometer (AAS) via filter sampling were for AuNP 19.34 ± 2.55 μg/m3 and AgNP 17.38 ± 1.88 μg/m3 for separate exposure and AuNP 8.20 ± 1.05 μg/m3 and AgNP 8.99 ± 1.77 μg/m3 for co-exposure. Lung retention and clearance were determined on day 1 (6-h) of exposure (E-1) and on post-exposure days 1, 7, and 28 (PEO-1, PEO-7, and PEO-28, respectively). While the AgNP and AuNP deposition rates were determined to be similar due to the similarity of NP size of both aerosols, the retention half-times and clearance rates differed due to the difference in dissolution rates. Thus, when comparing the lung burdens following separate exposures, the AgNP retention was 10 times less than the AuNP retention at 6-h (E-1), and 69, 89, and 121 times lower less than the AuNP retention at PEO-1, PEO-7, and PEO-28, respectively. In the case of AuNP+AgNP co-exposure, the retained AgNP lung burden was 14 times less than the retained AuNP lung burden at E-1, and 26, 43, and 55 times less than the retained AuNP lung burden at PEO-1, PEO-7, and PEO-28, respectively. The retention of AuNP was not affected by the presence of AgNP, but AgNP retention was influenced in the presence of AuNP starting at 24 h after the first day of post day of exposure. The clearance of AgNPs of the separate exposure showed 2 phases; fast (T1/2 3.1 days) and slow (T1/2 48.5 days), while the clearance of AuNPs only showed one phase (T1/2 .81.5 days). For the co-exposure of AuNPs+AgNPs, the clearance of AgNPs also showed 2 phases; fast (T1/2 2.2 days) and slow (T1/2 28.4 days), while the clearance of AuNPs consistently showed one phase (T1/2 54.2 days). The percentage of Ag lung burden in the fast and slow clearing lung compartment was different between separate and combined exposure. For the combined exposure, the slow and fast compartments were each 50% of the lung burden. For the single exposure, 1/3 of the lung burden was cleared by the fast rate and 2/3 of the lung burden by the slow rate.ConclusionsThe clearance of AgNPs follows a two- phase model of fast and slow dissolution rates while the clearance of AuNPs could be described by a one- phase model with a longer half-time. The co-exposure of AuNPs+AgNPs showed that the clearance of AgNPs was altered by the presence of AuNPs perhaps due to some interaction between AgNP and AuNP affecting dissolution and/or mechanical clearance of AgNP in vivo.

Project description:Background: Nickel oxide nanoparticles (NiO-NPs) have recently been utilized in various advanced industrial fields like lithium-ion micro batteries, nanofibers, electrochromic devices, and several biomedical applications. NiO-NPs are classified as extremely toxic substances as they can cause long-term harm to the environment and aquatic life. Moreover, frequent and prolonged exposure can affect human and animal health, causing skin allergies and major toxic consequences, such as hepatorenal toxicity. Hesperidin (HSP) has been proven to possess anti-inflammatory, antioxidant, and free radical scavenging activities. Objective: This study aimed to investigate the underlying protective mechanisms and effects of HSP against NiO-NPs-induced hepatorenal toxicities in rats. Materials and Methods: Forty male Wistar rats were randomly divided into four groups (n = 10 in each). The first group served as a Control group. For 8 weeks, the second group was administered NiO-NPs (100 mg/kg/day), and the third group was given HSP (100 mg/kg/day) via oral gavage for both groups. The fourth group received NiO-NPs and HSP concurrently in the same oral daily doses and duration as the second and third groups. Results: NiO-NPs administration revealed a significant increase in plasma biomarkers of nephrotoxicity (urea, creatinine) and hepatotoxicity (ALT, AST) in NiO-NPs group compared to Control group (p < 0.05). In addition, NiO-NPs administration resulted in a substantial increase in malondialdehyde levels with a significant drop in catalase activity and GSH content in Group II. Also, a significant decreased expression of Nrf-2 and Bcl-2 mRNA levels and upregulation of TNF-α, NF-kβ and BAX in the liver and kidney of NiO-NPs group were also detected. Histologically, the liver and kidney of rats of NiO-NPs group showed significant histopathological disturbances, with a substantial increase in the proliferating cell nuclear antigen (PCNA) positive hepatocytes and renal tubular cells in the NiO-NPs group compared to Control and HSP groups (p < 0.05). In contrast, concomitant administration of HSP with NiO-NPs in group IV showed a significant biochemical, histopathological, and immunohistochemical improvement compared to NiO-NPs group. Conclusion: Co-administration of HSP with NiO-NPs significantly ameliorated most of the NiO-NPs-induced hepatorenal toxicities in male rats.

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Looking for the LOAEL or NOAEL Concentration of Nickel-Oxide Nanoparticles in a Long-Term Inhalation Exposure of Rats.

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Looking for the LOAEL or NOAEL Concentration of Nickel-Oxide Nanoparticles in a Long-Term Inhalation Exposure of Rats.

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