Photosynthesis provides carbon sources and energy for crop growth and development, and the widespread presence of microplastics and plastic plasticisers in agricultural soils affects crop photosynthesis, but the mechanism of the effect is not clear. This study aims to investigate the effects of different microplastics and plasticizers on cucumber photosynthesis. Using polyvinyl chloride (PVC), polyethylene (PE), polystyrene (PS), and di-n-octyl phthalate (DOP) as representative microplastics and plasticizers, we assessed their impact on cucumber photosynthesis. Our results reveal significant alterations in key parameters: intercellular CO2 concentration (Ci) and transpiration rate (Tr) increased across all treatments, whereas stomatal limit value (Ls) and water use efficiency (WUE) decreased. Notably, PS + DOP treatment led to a significant reduction in the maximum efficiency of photosystem II (Fv/Fm) and ATP accumulation. Furthermore, PE and PS + DOP treatments decreased lycopene and ɛ-carotene synthesis rates, as well as abscisic acid (ABA) accumulation. All treatments inhibited the conversion of β-carotene into strigolactone (SL) and decreased chlorophyll synthesis rates, with PS + DOP exhibiting the most severe impact. Regarding chlorophyll degradation pathways, PVC and PE treatments reduced chlorophyll decomposition rates, whereas DOP with PS promoted degradation. PE and PS treatments also impaired light energy capture, electron transport, and the structural stability of photosystems I and II, as well as photosynthetic capacity and NADPH and ATP synthesis rates. Our findings underscore the differential impacts of microplastics and plasticizers on cucumber photosynthesis, with PS + DOP having the most detrimental effect. These results shed light on the complex interactions between microplastics and plant physiology, highlighting the urgent need for mitigation strategies in agricultural practices to safeguard crop productivity and environmental sustainability.

Di-(2-ethylhexyl) phthalate (DEHP) is the most commonly used phthalate and is ubiquitous in surface water. Based on its well-established toxicological profile, many countries and regions have adopted specific environmental quality standard (EQS) for DEHP. In China, the EQS value for DEHP is 8 μg/L. However, information on isomers structurally similar to DEHP is limited. Among the isomers of DEHP, di-isooctyl phthalate (DIOP) and di-n-octyl phthalate (DnOP) have received limited attention. The goal of this paper was to study effects and toxic potencies of DEHP, DIOP, and DnOP to individuals and predict effects on populations of female Daphnia magna (cladoceran crustacea) in media containing environmentally relevant concentrations of single PAEs for three consecutive generations (21 days for every generation). Exposure to all three PAEs resulted in reduced survival and reproduction and cause collapse of populations at the highest concentrations. DnOP was the most potent for causing adverse effects followed by DIOP, while DEHP was the least potent. 8 μg DnOP/L were found to reduce the population size by 37 % in the F2 generation. These findings demonstrate that PAE isomers other than DEHP can cause adverse effects.

Phthalic acid esters (PAEs) are commonly used as plasticizer and are emerging concern worldwide for potent adverse effects of aquatic organisms. Certain PAEs were often detected in different environmental matrices but related toxicity data were still lacking to support their risk assessment. The study investigated the acute toxicity of Diisobutyl phthalate (DiBP) and Di-n-octyl phthalate (DnOP) using 6 Chinese resident aquatic organisms from 3 phyla and 6 species and constructed the species sensitivity distribution (SSD) models for ecological risk assessment. Lethal concentration 50% (LC50) ranges of DiBP and DnOP were 4.89-21.45 mg/L and 1.45-1200 mg/L, respectively. The derived acute and chronic predicted no-effect concentrations (PNECs) based on log-normal model of water were 0.54 and 0.04 mg/L for DiBP and 0.23 and 0.05 mg/L for DnOP, respectively. The ERA for DiBP and DnOP in the surface water and sediment of China was conducted. Water samples of Haihe Rive (RQ = 0.41) and Hun River (RQ = 0.16) of DiBP showed medium risk. And sediment samples of Yellow River (RQ = 0.71) and Chao Hu Lake (RQ = 0.42) of DiBP showed medium risk. Meanwhile, the above water and sediment samples (RQ＜0.1) of DnOP showed low risk.

Humans are exposed to phthalates ubiquitously, which may threaten health. However, whether di-n-octyl phthalate can prevent pubertal sexual maturity is still elusive. In this study, male Sprague Dawley rats (age 35 days) were treated daily by gavage with 0, 10, 100, and 1000 mg/kg body weight of di-n-octyl phthalate from day 35 to day 49 after birth. Di-n-octyl phthalate significantly reduced serum testosterone levels at doses of 100 and 1000 mg/kg, but increased serum luteinizing hormone levels of 1000 mg/kg and decreased testosterone/luteinizing hormone ratio at ≥10 mg/kg, without affecting serum follicle-stimulating hormone levels. Di-n-octyl phthalate significantly induced Leydig cell hyperplasia (increased number of CYP11A1-positive Leydig cells) at 100 and 1000 mg/kg. Di-n-octyl phthalate down-regulates the gene expression of Cyp11a1, Hsd3b1 and Insl3 in individual Leydig cells. Di-n-octyl phthalate can also reduce the number of sperm in the epididymis. Di-n-octyl phthalate increased phosphorylated AKT1/AKT2 without affecting their total proteins, but increased the total protein and phosphorylated protein of ERK1/2 and GSK-3β. Primary immature Leydig cells isolated from 35-day-old rats were treated with 0-50 μM di-n-octyl phthalate for 3 h. This phthalate inhibited androgen production under basal, LH-stimulated, and cAMP-stimulated conditions by 5 and 50 μM in vitro via down-regulating Cyp11a1 expression but up-regulating Srd5a1 expression in vitro. In conclusion, di-n-octyl phthalate induces hypergonadotropic hypogonadism caused by Leydig cell hyperplasia but reduced steroidogenic function and prevents sperm production.

Di-n-octyl phthalate (DOP), a plasticizer used in many different industrial products, is a frequently observed pollutant in the environment. Biodegradation by microorganisms is considered to be a realistic choice for the remediation of DOP contamination. In the present research, the halotolerant bacterial consortium (LF) enriched in our previous research was used to degrade DOP. It was found that the optimal conditions for LF to degrade DOP was temperature 30oC, pH 6.0, inoculum size >5%, and salt content <3%. LF could degrade a high concentration of DOP (2000 mg/L) with the removal efficiency of 96.33%. Substrate inhibition analyses indicated that the inhibition constant, maximum specific degradation rate and half-saturation constant were 2544.6 mg/L, 0.7 d-1 and 59.1 mg/L, respectively. Based on the analysis of the gas chromatography-mass spectrometry (GC-MS), the biodegradation pathway for DOP by LF was proposed. Furthermore, LF could degrade DOP in soil (100 mg/kg) with the highest removal efficiency of 89.3%. This study is the first report on DOP biodegradation by bacterial consortium. These results suggest that LF can be used to remediate DOP-contaminated environment.