With the widespread use of pesticides, the resistance to pesticides of pests has gradually increased, caused mixed pesticides to become even more widely used for practical applications. To investigate the effects of mixed pesticides on reproductive health in an occupational greenhouse environment, the greenhouse environment and the characteristics of the actual application were constructed, and then the male mice were comprehensively exposed to a mixture of the beta-cypermethrin and emamectin benzoate environmental. Additionally, the effect of the beta-cypermethrin and emamectin benzoate mixture on the reproductive health of male mice was known. The results showed that with the prolongation of exposure duration, the activities of Glutathione Peroxidase (GSH-Px), Total Superoxide Dismutase (T-SOD), Lactate dehydrogenase (LDH) and Acid phosphatase (ACP) in the testes of mice gradually decreased and the activity of Malondialdehyde (MDA) gradually increased. It was also found that the apoptosis rate of murine testicular cells increased and that DNA damage occurred with prolonged exposure duration. Therefore, it can be inferred that exposure to a mixture of the pesticides beta-cypermethrin and emamectin benzoate in the greenhouse environment may have adverse effects on the reproductive health of male mice.

Rare ginsenosides have already been widely applied in many fields, including health food and bio-medicine. The human being can expose to rare ginsenosides directly or indirectly increasingly. However, there are few studies on the safety assessment of rare ginsenoside mixtures. In the present study, the sub-chronic toxicity of rare ginsenosides for 90 days on SD rats was performed by combining the intestinal flora analysis and urine metabonomics aiming to illustrate the safety of long-term consumption of rare ginsenosides and the potential damage for liver and intestinal. 48 adult rats were divided into four groups: control (0 mg/kg), low-dose (60 mg/kg), medium-dose (200 mg/kg), and high-dose (600 mg/kg). Rats in the high-dose group showed inflammatory changes in their livers and intestines. The strong bactericidal effect of rare ginsenosides caused intestinal flora disorder and changed the structure of intestinal flora in rats, thus inducing intestinal damage in rats. In the high-dose group, levels of alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and alkaline phosphatase (AKP) increased significantly. As a result of the high-dose treatment, certain metabolic pathways were altered, such as vitamin B6 metabolism, methionine metabolism, glutathione metabolism, and others. These results indicated that high doses of rare ginsenosides induced liver injury by affecting the above metabolic pathways. Rare ginsenosides with no observed adverse effect level (NOAEL) were below 200 mg/kg/day in vivo. Thus, this present study provides insight into the rational use of rare ginsenosides.

The ubiquitous presence of micro- and nano-plastics (MNPs) has made their pollution a global concern, as it leads to human exposure. Dietary exposure represents a major route for human exposure to MNPs, which have the potential to impact human health. This paper aims to review the source, occurrence, characteristics, and analytical methods of MNPs in food. The challenges and limitations involved in assessing the human health risks associated with MNPs through food consumption were also discussed. Studies have found that various foods, particularly seafood, are contaminated with MPs. However, limited data are available on MPs in other commonly consumed food items such as meat, vegetables, and fruits. Furthermore, there is a lack of investigation into the characteristics of nanoplastics (NPs, <1 µm) and oligomer polymers (low molecular weight polymers) which are more prone to entering human body because of smaller sizes. MNPs are possibly introduced into food through different pathways, including raw food materials, food processing and production, packaging and containers, as well as preparation and dining processes. The complexity of food matrix poses challenges to the development of methodologies to investigate MNPs, hindering comprehensive data acquisition and human exposure assessment. Additionally, the lack of epidemiological, clinical, and toxicological data related to environmental MNPs makes it difficult to conduct accurate hazard identification and characterization. These limitations impede the feasibility of conducting health risk assessment. Therefore, we urgently call for a better understanding of health risks of MNPs, achieved through the improvement of methodologies and the expansion of available data.

Parkinson’s disease (PD) is a complex neurodegenerative disorder characterized by a pathology that includes the aggregation of alpha-synuclein (α-syn), oxidative stress, and neuroinflammation. While existing treatments can alleviate motor symptoms, they have limited efficacy in slowing disease progression and improving non-motor symptoms. In recent years, molecular hydrogen has been recognized for its potential neuroprotective effects, attributed to its selective antioxidant and anti-inflammatory properties. While preclinical studies demonstrate promising results, clinical trials conducted thus far have yielded mixed outcomes, with some trials reporting limited or no therapeutic benefit. This review systematically analyzes the mechanisms of action of molecular hydrogen in PD and related neurodegenerative disorders, emphasizing its antioxidant, anti-inflammatory, and anti-apoptotic properties. By evaluating evidence from both preclinical and clinical studies, this paper explores the potential of molecular hydrogen to attenuate oxidative stress, modulate inflammatory responses, and inhibit apoptosis in neuronal cells, while also identifying key gaps in current research. As a novel neuroprotective agent, molecular hydrogen holds potential in PD and other neurodegenerative diseases, but further well-designed clinical trials are needed to validate its efficacy. Future studies should focus on elucidating the mechanisms through which hydrogen exerts its neuroprotective effects, particularly concerning α-syn aggregation and its clearance pathways, as well as Nrf2-mediated immunomodulation. Furthermore, large-scale, multicenter clinical trials are necessary to establish efficacy benchmarks and personalized delivery protocols.