Simeprevir induces ferroptosis through ß-TrCP/Nrf2/GPX4 axis in triple-negative breast cancer cells.

The effective treatment regimens of triple-negative breast cancer (TNBC), a specific subtype of breast cancer (BC) with proneness to relapse and poor prognosis, are still lacking. Simeprevir (SIM), approved for hepatitis C infection treatment, has been proved to be a competitive drug for the treatment of various solid tumors recently. However, the anti-tumor mechanisms of SIM and therapeutic effects on TNBC are uncertain. In this study, we suggested that SIM effectively restrained the growth of MDA-MB-231 and BT-549 cells, two cell lines from TNBC. The RNA sequencing revealed that ferroptosis signaling was activated in SIM-treated TNBC cells. SIM induced ferroptosis in TNBC cells through reduced glutathione (GSH) levels, increased iron levels, ROS and lipid peroxidation. Mechanistically, SIM promoted the expression of ß-TrCP to inhibit the Nrf2/GPX4 axis in TNBC cells, leading to ferroptosis. Moreover, SIM administration into the xenografts formed by MDA-MB-231 dramatically suppressed the tumor progression by inducing ferroptosis in vivo. Collectively, this finding reveals that SIM may serve as a competitive therapeutic strategy to inhibit TNBC.

EGR1 Promotes Erastin-induced Ferroptosis Through Activating Nrf2-HMOX1 Signaling Pathway in Breast Cancer Cells.

Purpose: Early growth response 1 (EGR1) is a crucial transcription factor composed of zinc finger structures, inhibitory and activating regulatory regions. We identified the biological effect and molecular mechanisms of EGR1 in breast cancer (BC). Methods: We used qRT-PCR, western blot and immunohistochemistry to examine the expression of EGR1 in BC samples. CCK-8 and colony assay were performed to reveal the effect of EGR1 on the proliferation of BC cells. LDH release assay, MCB assay, MDA assay, C-AM assay and TMRE assay were performed to measure the levels of LDH release, GSH, MDA, LIP and mitochondrial membrane potential. The regulation of EGR1 on the expression of Nrf2 and HMOX1 was investigated through Western blot. Xenograft models were conducted to determine the impact of EGR1 overexpression on BC in vivo. Results: The expression of EGR1 was downregulated in BC tissues compared with the normal tissues, and lower expression of EGR1 associated with poorer clinical outcome in BC patients. Through in vitro experiments, we found that EGR1 downregulation facilitated the proliferation of BC cells, and overexpression of EGR1 inhibited the proliferation of BC cells. In addition, EGR1 knockdown alleviated erastin-induced ferroptosis and overexpression of EGR1 facilitated erastin-induced ferroptosis in BC cells. Moreover, overexpression of EGR1 facilitated the anti-tumor effect caused by erastin in vivo. Mechanistically, the phosphorylation levels of Nrf2 and the expression of HMOX1 were reduced due to the downregulation of EGR1, and increased due to the upregulation of EGR1. Additionally, the finding that EGR1 facilitated erastin-induced ferroptosis was alleviated by the inhibition of Nrf2-HMOX1. Conclusion: The expression of EGR1 is downregulated in BC, which is correlated with poor prognosis of BC patients. EGR1 suppresses the proliferation of BC cells and facilitates erastin-induced ferroptosis by activating Nrf2-HMOX1 signaling pathway in BC cells.

LSD2 Is an Epigenetic Player in Multiple Types of Cancer and Beyond.

Histone demethylases, enzymes responsible for removing methyl groups from histone proteins, have emerged as critical players in regulating gene expression and chromatin dynamics, thereby influencing various cellular processes. LSD2 and LSD1 have attracted considerable interest among these demethylases because of their associations with cancer. However, while LSD1 has received significant attention, LSD2 has not been recognized to the same extent. In this study, we conduct a comprehensive comparison between LSD2 and LSD1, with a focus on exploring LSD2's implications. While both share structural similarities, LSD2 possesses unique features as well. Functionally, LSD2 shows diverse roles, particularly in cancer, with tissue-dependent roles. Additionally, LSD2 extends beyond histone demethylation, impacting DNA methylation, cancer cell reprogramming, E3 ubiquitin ligase activity and DNA damage repair pathways. This study underscores the distinct roles of LSD2, providing insights into their contributions to cancer and other cellular processes.

FTO demethylates regulates cell-cycle progression by controlling CCND1 expression in luteinizing goat granulosa cells.

In mammals, N6-methyladenosine (m6A) stands out as one of the most abundant internal mRNA modifications and plays a crucial role in follicular development. Nonetheless, the precise mechanism by which the demethylase FTO regulates the progression of the goat luteinizing granulosa cells (LGCs) cycle remains to be elucidated. In our study, we primarily assessed the protein and mRNA expression levels of genes using Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR), cell proliferation via EdU, cell viability with CCK-8, and apoptosis and cell cycle progression through flow cytometry. Here, the results demonstrated that knockdown of FTO significantly enhanced apoptosis, impeded cell proliferation, and increased autophagy levels in goat LGCs. Furthermore, the silencing of FTO substantially reduced cyclin D1 (CCND1) expression through the recognition and degradation of YTHDF2, consequently prolonging the cell cycle progression. This study sheds light on the mechanism by which FTO demethylation governs cell cycle progression by controlling the expression of CCND1 in goat LGCs, underscoring the dynamic role of m6A modification in the regulation of cell cycle progression.

N6-methyladenosine methyltransferase METTL3 modulates the cell cycle of granulosa cells via CCND1 and AURKB in Haimen goats.

N6-methyladenosine (m6A) plays a crucial role in many bioprocesses across species, but its function in granulosa cells during oocyte maturation is not well understood in animals, especially domestic animals. We observed an increase in m6A methyltransferase-like 3 (METTL3) in granulosa cells during oocyte maturation in Haimen goats. Our results showed that knockdown of METTL3 disrupted the cell cycle in goat granulosa cells, leading to aggravated cell apoptosis and inhibition of cell proliferation and hormone secretion. Mechanistically, METTL3 may regulate the cell cycle in goat granulosa cells by mediating Aurora kinase B (AURKB) mRNA degradation in an m6A-YTH N6-methyladenosine RNA binding protein 2 (YTHDF2) manner and participating in AURKB transcription via the Cyclin D1 (CCND1)-Retinoblastoma protein (RB)-E2F transcription factor 1 (E2F1) pathway. Overall, our study highlights the essential role of METTL3 in granulosa cells during oocyte maturation in Haimen goats. These findings provide a theoretical basis and technical means for understanding how RNA methylation participates in oocyte maturation through granulosa cells.

chi-miR-130b-3p regulates the ZEA-induced oxidative stress damage through the KEAP1/NRF2 signaling pathway by targeting SESN2 in goat GCs.

As a dominant mycotoxin, zearalenone (ZEA) has attracted extensive attention due to its estrogen-like effect and oxidative stress damage in cells. In order to find a way to relieve cell oxidative stress damage caused by ZEA, we treated goat granulosa cells (GCs) with ZEA and did a whole transcriptome sequencing. The results showed that the expression level of Sesterin2 (SESN2) was promoted extremely significantly in the ZEA group (p < .01). In addition, our research demonstrated that SESN2 could regulate oxidative stress level in GCs through Recombinant Kelch Like ECH Associated Protein 1 (KEAP1)/Nuclear factor erythroid 2-related factor 2 (NRF2) signaling pathway. The overexpression of SESN2 could reduce the oxidative damage, whereas knockdown of SESN2 would aggravate the oxidative damage caused by ZEA. What's more, microRNA (miRNA) chi-miR-130b-3p can bind to SESN2 3'-untranslated region (3'UTR) to regulate the expression of SESN2. The mimics/inhibition of chi-miR-130b-3p would have an effect on oxidative damage triggered by ZEA in GCs as well. In summary, these results elucidate a new pathway by which chi-miR-130b-3p affects the KEAP1/NRF2 pathway in GCs by modulating SESN2 expression in response to ZEA-induced oxidative stress damage.

miR-101-5p overexpression suppresses the proliferation of goat spermatogonial stem cells by targeting EZH2.

MicroRNAs (miRNAs), as post-transcriptional gene mediators, regulate the biological characteristics of spermatogonial stem cells (SSCs), including proliferation, differentiation and apoptosis. However, the potential roles and mechanisms by which miR-101-5p affected the biological characters of goat SSCs have not been fully elucidated. Herein, we reported that miR-101-5p overexpression decreased cell viability (P < 0.01), arrested cell cycle in the G1 phase (P < 0.05), and aggravated apoptosis of goat SSCs (P < 0.01) compared with negative control (NC), as determined by CCK-8 assay and flow cytometry analysis. Additionally, PCNA protein expression was attenuated by miR-101-5p overexpression (P < 0.05). Notably, the expression of SSCs specific genes Oct4 (P < 0.05), PLZF (P < 0.01) and DAZL (P < 0.01) were decreased in miR-101-5p overexpressed SSCs. Furthermore, the dual luciferase reporter assay showed that, when co-transfected with miR-101-5p mimics, the relative luciferase activity of EZH2 wide-type (WT) was inhibited (P < 0.05) compared with the transfection of EZH2 mutant (MUT). EZH2 expression was negatively correlated with miR-101-5p expression in goat SSCs. Collectively, our data implicates that miR-101-5p overexpression aggravates cell apoptosis, and suppresses cell proliferation of goat SSCs via targeting EZH2, which may impair spermatogenesis.

CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype.

The heterogeneity of cancer-associated fibroblasts (CAFs) might be ascribed to differences in origin. CD10 and GPR77 have been reported to identify a chemoresistance-inducing CAF subset in breast cancer. However, the precise mechanism for the formation of the CD10+GPR77+ CAFs remains unknown. In this study, we found that CCL18 expression was positively correlated with the density of CD10+GPR77+ CAFs in breast cancer and associated with a poor response to chemotherapy. Moreover, CCL18 secreted by tumor-associated macrophages (TAMs) activated a CD10+GPR77+ CAF phenotype in normal breast-resident fibroblasts (NBFs), which could then enrich cancer stem cells (CSCs) and induce chemoresistance in breast cancer cells. Mechanistically, CCL18 activated NF-κB signaling via PITPNM3 and thus enhanced the production of IL-6 and IL-8. Furthermore, intratumoral CCL18 injection significantly induced the activation of NBFs and the chemoresistance of xenografts in vivo. In addition, targeting CCL18 by anti-CCL18 antibody could inhibit the formation of CD10+GPR77+ CAFs and recover the chemosensitivity in vivo, leading to effective tumor control. Collectively, these findings reveal that inflammatory signaling crosstalk between TAMs and fibroblasts is responsible for the formation of the CD10+GPR77+ CAFs, suggesting CCL18-PITPNM3 signaling is a potential therapeutic target to block the activation of this specific CAF subtype and tumor chemoresistance.

The function of the m6A methyltransferase METTL3 in goat early embryo development under hypoxic and normoxic conditions.

It has been reported that N6-methyladenosine (m6A) methyltransferase-like 3 (METTL3) plays an important role in zygote genome activation during embryonic development, but the effects of METTL3 under oxidative stress in the early development of goat embryos remain largely unknown. In this study, zygotes were monitored at 72 and 168 h after fertilization, and they developed to the 8-cell stage and blastocyst stage under hypoxic conditions and normoxic conditions. Single-cell transcriptome sequencing was performed at the 8-cell stage and the blastocyst stage in the goat embryos, the differentially expressed METTL3 was screened from the sequencing results. We found that microinjection of small interfering RNA (siRNA) against METTL3 caused developmental arrest, both 8-cell rates (37.45 ± 2.21% vs. 47.09 ± 1.38%; P < 0.01) and blastocyst rates of Si-METTL3 (12.17% ± 2.84 vs. 20.83 ± 3.61%; P < 0.01) in Si-METTL3 group were significantly decreased compared with that of control under hypoxic conditions, significant changes were found in the m6A-related genes and the expression levels of critical transcription factors, such as, NANOG, GATA3, CDX2 and SOX17, were decreased. This study revealed the key role of METTL3 in the regulation of embryonic development under oxidative stress, and laid the foundation for further study of the crucial mechanism of oxidative stress during the early embryonic development of goats.

Effects of dietary betaine supplementation on biochemical parameters of blood and testicular oxidative stress in Hu sheep.

Betaine, a highly valuable feed additive, has been observed to alter the distribution of protein and fat in the bodies of ruminants and to exhibit strong antioxidant properties. However, the effects of dietary betaine supplementation on the biochemical parameters of blood and on testicular oxidative stress remain unknown. This study aimed to investigate the effects of dietary betaine supplementation on lipid metabolism, immunity, and testicular oxidative status in Hu sheep. Experimental sheep (n=3, three sheep per group) were fed betaine-containing diets, a basal diet supplemented with 0 g/day (control group), 1 g/day (B1), and 3 g/day betaine (B2). There were no differences in the serum concentrations of triglycerides and cholesterol in Hu sheep receiving diets supplemented with betaine. The ratio of basophils significantly increased in the B1 and B2 groups. ELISA (enzyme-linked immunosorbent assay) results showed that testicular superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity were significantly higher, whereas malondialdehyde (MDA) content significantly decreased, after feeding betaine-supplemented diets. qPCR results showed that the mRNA expression levels of CAT, SOD2, and GSH-Px were significantly upregulated in both the B1 and B2 groups compared to those in the control group. Furthermore, the expression of proliferating cell nuclear antigen (PCNA) was significantly lower in the testes of betaine-treated Hu sheep than in the control group. Moreover, LKB1 (liver kinase B1) expression significantly increased, and mRNA expression of AMPK (AMP-activated serine/threonine protein kinase) significantly decreased in the B1 group. The relative gene expression of mTOR (mechanistic target of rapamycin) was significantly higher in the B2 group than in the control group. RAPTOR expression significantly increased in the B1 group. Western blot revealed that the ratio of P-mTOR and mTOR significantly increased after feeding betaine-supplemented diets. In conclusion, betaine supplementation improved serum lipid metabolism, immune response, and increased the testicular antioxidant capacity of Hu sheep, which might be regulated via mTOR signaling pathway.

Effects of l-arginine on endometrial estrogen receptor α/ß and progesterone receptor expression in nutrient-restricted sheep.

This study aimed to determine the effects of l-arginine (L-Arg) supplementation on steroid hormone receptors in non-pregnant ovine endometrium. All experimental ewes were randomly assigned to either a control group (n = 6), a nutrient-restricted group (n = 6), or an L-Arg supplemented nutrient-restricted group (n = 6). The effects of L-Arg on estrogen receptor α/ß (ERα/ß) and progesterone receptor (PGR) expression in the ovine endometrium were assessed. Our results showed that levels of ERß and PGR expression were significantly increased by nutrient restriction, but L-Arg counteracted the effect of nutrient restriction on ERß and PGR expression (p < 0.05). Also, expression of endometrial ERα was substantially increased (p < 0.05) by L-Arg supplementation. Furthermore, ERα/ß and PGR were mainly detected in the endometrial luminal epithelium and glandular epithelium. Therefore, we isolated and identified endometrial epithelial cells (EECs) from sheep. Different concentrations of L-Arg were added to investigate the effects on ERα/ß and PGR in EECs. The expression levels of endothelial nitric oxide synthase, ERß, and PGR were significantly increased in response to low-concentration (200 µmol) L-Arg supplementation, which subsequently decreased with a high concentration (800 µmol) (p < 0.05). Otherwise, ERα expression was remarkably increased at both L-Arg concentrations in EECs (p < 0.05). Overall, the results indicated that L-Arg performed crucial roles in the regulation of ovine steroid hormone receptor expression in the endometrium. The results of this study provide a theoretical basis and technical means for the normal function of endometrium in response to low nutrient levels.

Effect of thyme essential oil against Bacillus cereus planktonic growth and biofilm formation.

The objective of this study was to determine the effect of thyme essential oil (TEO) on the planktonic growth and biofilm formation of Bacillus cereus (B. cereus). GC-MS analysis of TEO allowed the detection of 13 compounds, and the major constituents were p-cymene (29.7%), thymol (23.73%), γ-terpinene (16.21%), and 1,8-cineole (9.74%). TEO exhibited a minimum inhibitory concentration (MIC) value against planktonic B. cereus of 0.25 mg/mL. The potent effect of TEO to inhibit the growth of planktonic B. cereus was due to cell membrane damage, as evidenced by reduced cell viability, protein changes, decreased intracellular ATP concentration, increased extracellular ATP concentration and cell membrane depolarization, and cellular morphological changes. In addition, TEO exerted a significant inhibitory effect on B. cereus biofilm formation, as confirmed by environmental scanning electron microscopic images. These findings suggested that TEO has the potential to be developed as a natural food additive to control foodborne contamination associated with B. cereus and its biofilm.

In vitro influence of selenium on the proliferation of and steroidogenesis in goat luteinized granulosa cells.

In this study, we investigated the effects of Selenium (Se) on the proliferation of and steroidogenesis in goat luteinized granulosa cells (LGCs) and elucidated the mechanisms underlying these effects. Our results showed that proliferating cell nuclear antigen (PCNA), Akt, and phosphoinositide 3-kinase (PI3K) were expressed mainly in ovarian oocytes and granulosa cells (GCs). We observed that 5 ng/mL Se significantly stimulated LGC proliferation, which could be attributed to increases in PCNA, cyclin-dependent kinase 1 (CDK1), phosphorylated adenosine monophosphate-activated protein kinase (p-AMPK; Thr172), and phosphorylated Akt (p-Akt; Ser473) and decreases in p21 (P < 0.05). Se treatment also significantly increased estradiol (E2) production, which could be, at least partially, due to increased levels of 3ß-hydroxysteroid dehydrogenase(3ß-HSD), steroidogenic acute regulatory protein (StAR), p-Akt (Ser473), and cyclic adenosine monophosphate (cAMP) (P < 0.05); however, follicle-stimulating hormone (FSH) significantly enhanced the production of E2, progesterone (P4) and cAMP (P < 0.05). Moreover, Se treatment stimulated proliferation and the synthesis of E2 and cAMP in the presence of FSH (P < 0.05). Additionally, the expression of antioxidant-related genes [glutathione peroxidase (GSH-Px) and superoxide dismutase 2 (SOD2)] and the activity of GSH-Px and SOD were progressively elevated by Se treatment (P < 0.05). These data suggested that Se plays an important role in the proliferation of and steroidogenesis in LGC by activating the PI3K/Akt and AMPK pathways, thereby increasing the expression of its downstream cell-cycle- and steroid-synthesis-related genes, as well as regulating cellular oxidative stress.

Vitamin D receptor expression and potential role of vitamin D on cell proliferation and steroidogenesis in goat ovarian granulosa cells.

This study aimed to investigate the expression of the vitamin D receptor (VDR) in goat follicles and to determine the effects of Vit D3 supplementation on goat granulosa cells (GCs) function linked to follicular development. The results demonstrated that VDR was prominently localized in GCs, with expression increasing with follicle diameter. Addition of Vit D3 (1α,25-(OH)2VD3; 10 nM) to GCs caused an increase in VDR and in steroidogenic acute regulator (StAR) and 3ß-hydroxysteroid dehydrogenase (3ß-HSD) mRNA expression. Additionally, Vit D3 increased the cyclic adenosine monophosphate (cAMP), estradiol (E2), and progesterone (P4) levels, while it decreased anti-müllerian hormone receptor (AMHR) and follicle-stimulating hormone receptor (FSHR) mRNA expression (P < 0.05). Addition of FSH remarkably increased E2, P4, and cAMP levels (P < 0.05), and Vit D3 further enhanced the E2 and cAMP levels in the presence of FSH (P < 0.05). Vit D3 significantly induced the mRNA expression of CDK4 and CyclinD1, and downregulated P21 gene expression (P < 0.05). In addition, Vit D3 significantly decreased reactive oxygen species (ROS) production and increased the mRNA and protein expression of superoxide dismutase 2 (SOD2) and catalase (CAT) (P < 0.05). In conclusion, VDR is expressed in GCs of the goat ovaries and Vit D3 might play an important role in GCs proliferation by regulating cellular oxidative stress and cell cycle-related genes. Meanwhile, Vit D3 enhances the E2 and P4 output of GCs by regulating the expression of 3ß-HSD and StAR and the level of cAMP, which regulate steroidogenesis, supporting a potential role for Vit D3 in follicular development.

Gas emissions from dairy cows fed typical diets of Midwest, South, and West regions of the United States.

Gas emissions were determined for dairy cows fed three diets formulated to represent feed ingredients typical of the Midwest, South, or West regions of the United States. Dairy cows were housed and monitored in 12 environmentally controlled rooms (4 cows diet). Two experiments were performed, representing two lactation stages (initial days in milk were 115 ± 39 d in Stage 1 and 216 ± 48 d in Stage 2). The results demonstrated that the combination of different dietary ingredients resulted in different gas emissions while maintaining similar dry matter intake (DMI) and milk yield (MY). Diet effect on ammonia (NH) emissions was more prominent in Stage 1. During Stage 1, cows fed the Midwest diet had the highest daily NH emission, corresponding to the highest crude protein (CP) concentration among the three regions. The differences in NH emissions (39.0%) were much larger than the percent difference in CP concentrations between diets (6.8%). Differences in N intake, N excretion, or milk urea N alone may not serve as a strong indicator of the potential to reduce NH emissions. Lower emissions of methane (CH) per unit DMI or per unit MY were observed for cows offered the South diet during Stage 1 as compared with that from cows offered the Midwest or West diets. No diet effect was observed for hydrogen sulfide (HS) emission per unit S intake, nor for nitrous oxide (NO) emission. The measured NH and CH emissions were comparable, but the NO emissions were much higher than those reported for tie-stall dairy barns in the literature.

Determination of polycyclic aromatic sulfur heterocycles in diesel particulate matter and diesel fuel by gas chromatography with atomic emission detection.

The sulfur content of diesel fuel is of environmental concern because sulfur can facilitate the formation of diesel particulate matter (DPM) and sulfur dioxide (SO2) in the exhaust can poison catalytic converters. The US Environmental Protection Agency (EPA) has established more stringent regulations to reduce the sulfur content of diesel fuels in the near future. In this study, various types of organosulfur compounds in DPM extracts and the corresponding fuels have been determined by gas chromatography with atomic emission detection. The diesel fuels used have sulfur contents of 2284 and 433 ppm, respectively, and are labeled as high-sulfur and low-sulfur diesel fuels. The compounds identified are mainly polycyclic aromatic sulfur heterocycles (PASHs). In the fuels tested, trimethylbenzothiophenes (TMBTs), dibenzothiophenes (DBTs), and 4-methyldibenzothiophene (4-MDBT) were the most abundant sulfur compounds, while larger PASH compounds were more abundant in DPM extracts. The high-sulfur diesel fuel contained a larger proportion of PASHs with one or two rings (lighter PASHs). In DPM, the concentrations of total organic sulfur and individual PASHs are higher for the high-sulfur diesel fuel, and the relative percentage of one or two-ring PASHs is higher as well. The influence of engine load on the DPM composition was also examined. With increasing load, the PASH concentration in DPM decreased for lighter PASHs, increased for heavier PASHs, and had a bell-shaped distribution for PASHs in between.

Variations of the particulate carbon distribution from a nonroad diesel generator.

The emissions of diesel particulate matter (DPM) from diesel engines are causing increasing health concerns due to their suspected carcinogenicity, especially the carbonaceous fractions. The total DPM emissions and the organic and elemental carbon (OC and EC) distributions of the DPM depend on many operating factors, such as load, engine design parameters, fuel sulfur content, fuel usage rate, and sampling conditions. Results of previous studies on the OC/EC variations with load for heavy-duty vehicles have been reported, but information is scarce for nonroad diesel generators. There is a clear need to better characterize nonroad DPM emissions, as studies have indicated that DPM emissions from nonroad diesel engines are significantly higher than those from on-road sources. The objective of the study is to provide a detailed account of the OC/EC distributions for a nonroad diesel generator operated with high and low sulfur fuels under different load conditions. DPM emissions were collected using an EPA Method 5 (Determination of Particulate Matter Emissions from Stationary Sources) sampling train. The OC and EC concentrations were quantified by NIOSH Method 5040. DPM concentrations and the relative contributions of OC, EC, and noncarbonaceous materials vary significantly with engine load, fuel sulfur content, and sample collection temperature. The fractions of EC over DPM increase with increasing load from 21% at OkW to 84% at 75 kW for the low sulfur fuel, while those of OC decrease from 62% to 9%. This is consistent with other studies, and the same trends exist regardless of the sulfur content and DPM collection temperature. The fractions of organic compounds range from 77% to 19% for the high sulfur fuel. Noncarbonaceous materials are from 27% to 18% in fraction from high sulfur DPM as opposed to the 17% to 7% in the low sulfur diesel emissions. At lower collection temperatures, more OC and noncarbonaceous materials are observed.

The organic composition of diesel particulate matter, diesel fuel and engine oil of a non-road diesel generator.

Diesel-powered equipment is known to emit significant quantities of fine particulate matter to the atmosphere. Numerous organic compounds can be adsorbed onto the surfaces of these inhalable particles, among which polycyclic aromatic hydrocarbons (PAHs) are considered potential occupational carcinogens. Guidelines have been established by various agencies regarding diesel emissions and various control technologies are under development. The purpose of this study is to identify, quantify and compare the organic compounds in diesel particulate matter (DPM) with the diesel fuel and engine oil used in a non-road diesel generator. Approximately 90 organic compounds were quantified (with molecular weight ranging from 120 to 350), which include alkanes, PAHs, alkylated PAHs, alkylbenzenes and alkanoic acids. The low sulfur diesel fuel contains 61% alkanes and 7.1% of PAHs. The identifiable portion of the engine oil contains mainly the alkanoic and benzoic acids. The composition of DPM suggests that they may be originated from unburned diesel fuel, engine oil evaporation and combustion generated products. Compared with diesel fuel, DPM contains fewer fractions of alkanes and more PAH compounds, with the shift toward higher molecular weight ones. The enrichment of compounds with higher molecular weight in DPM may be combustion related (pyrogenic).