Biodegradation of Typical Plastics: From Microbial Diversity to Metabolic Mechanisms.

Plastic production has increased dramatically, leading to accumulated plastic waste in the ocean. Marine plastics can be broken down into microplastics (<5 mm) by sunlight, machinery, and pressure. The accumulation of microplastics in organisms and the release of plastic additives can adversely affect the health of marine organisms. Biodegradation is one way to address plastic pollution in an environmentally friendly manner. Marine microorganisms can be more adapted to fluctuating environmental conditions such as salinity, temperature, pH, and pressure compared with terrestrial microorganisms, providing new opportunities to address plastic pollution. Pseudomonadota (Proteobacteria), Bacteroidota (Bacteroidetes), Bacillota (Firmicutes), and Cyanobacteria were frequently found on plastic biofilms and may degrade plastics. Currently, diverse plastic-degrading bacteria are being isolated from marine environments such as offshore and deep oceanic waters, especially Pseudomonas spp. Bacillus spp. Alcanivoras spp. and Actinomycetes. Some marine fungi and algae have also been revealed as plastic degraders. In this review, we focused on the advances in plastic biodegradation by marine microorganisms and their enzymes (esterase, cutinase, laccase, etc.) involved in the process of biodegradation of polyethylene terephthalate (PET), polystyrene (PS), polyethylene (PE), polyvinyl chloride (PVC), and polypropylene (PP) and highlighted the need to study plastic biodegradation in the deep sea.

Continuous generation and release of microplastics and nanoplastics from polystyrene by plastic-degrading marine bacteria.

Plastic waste released into the environments breaks down into microplastics due to weathering, ultraviolet (UV) radiation, mechanical abrasion, and animal grazing. However, little is known about the plastic fragmentation mediated by microbial degradation. Marine plastic-degrading bacteria may have a double-edged effect in removing plastics. In this study, two ubiquitous marine bacteria, Alcanivorax xenomutans and Halomonas titanicae, were confirmed to degrade polystyrene (PS) and lead to microplastic and nanoplastic generation. Biodegradation occurred during bacterial growth with PS as the sole energy source, and the formation of carboxyl and carboxylic acid groups, decreased heat resistance, generation of PS metabolic intermediates in cultures, and plastic weight loss were observed. The generation of microplastics was dynamic alongside PS biodegradation. The size of the released microplastics gradually changed from microsized plastics on the first day (1344 nm and 1480 nm, respectively) to nanoplastics on the 30th day (614 nm and 496 nm, respectively) by the two tested strains. The peak release from PS films reached 6.29 × 106 particles/L and 7.64 × 106 particles/L from degradation by A. xenomutans (Day 10) and H. titanicae (Day 5), respectively. Quantification revealed that 1.3% and 1.9% of PS was retained in the form of micro- and nanoplastics, while 4.5% and 1.9% were mineralized by A. xenomutans and H. titanicae at the end of incubation, respectively. This highlights the negative effects of microbial degradation, which results in the continuous release of numerous microplastics, especially nanoplastics, as a notable secondary pollution into marine ecosystems. Their fates in the vast aquatic system and their impact on marine lives are noted for further study.

Biodegradation of polyethylene terephthalate (PET) by diverse marine bacteria in deep-sea sediments.

PET plastic waste entering the oceans is supposed to take hundreds of years to degrade and tends to accumulate in the deep sea. However, we know little about the bacteria capable of plastic degradation therein. To determine whether PET-degrading bacteria are present in deep-sea sediment, we collected the samples from the eastern central Pacific Ocean and initiated microbial incubation with PET as the carbon source. After enrichment with PET for 2 years, we gained all 15 deep-sea sediment communities at five oceanic sampling sites. Bacterial isolation for pure culture and further growth tests confirmed that diverse bacteria possess degradation ability including Alcanivorax xenomutans BC02_1_A5, Marinobacter sediminum BC31_3_A1, Marinobacter gudaonensis BC06_2_A6, Thalassospira xiamenensis BC02_2_A1 and Nocardioides marinus BC14_2_R3. Furthermore, four strains were chosen as representatives to reconfirm the PET degradation capability by SEM, weight loss and UPLC-MS. The results showed that after 30-day incubation, 1.3%-1.8% of PET was lost. De-polymerization of PET by the four strains was confirmed by the occurrence of the PET monomer of MHET and TPA as the key degradation products. Bacterial consortia possessing PET-degrading potential are prevalent and diverse and might play a key role in the removal of PET pollutants in deep oceans.

Highly efficient actively Q-switched Nd:YAG laser.

A novel gain medium structure is designed providing Q-switched pulses with high efficiency. The use of an improved corner-side hybrid pump structure achieves a high absorption efficiency of pump light by crossing through the active media 13 times Nd:YAG. A layer of Sm:YAG is bonded around the active media, which suppresses parasitic oscillation and amplified spontaneous emission (ASE) effectively. A high-efficient actively Q-switched laser is successfully realized with a pulse energy of 104 mJ. The corresponding optical-optical conversion efficiency is 30.5%. This is, to the best of our knowledge, the highest optical to optical efficiency for an actively Q-switched Nd:YAG laser at the hundred milli-joules level.

Betaine supplementation attenuates atherosclerotic lesion in apolipoprotein E-deficient mice.

BACKGROUND: Betaine serves as a methyl donor in a reaction converting homocysteine to methionine. It is commonly used for the treatment of hyperhomocysteinemia in humans, which indicates it may be associated with reduced risk of atherosclerosis. However, there have been few data regarding its vascular effect. AIM OF THE STUDY: To investigate the effect of betaine supplementation on atherosclerotic lesion in apolipoprotein (apo) E-deficient mice. METHODS: Four groups of apoE-deficient mice were fed AIN-93G diets supplemented with 0, 1, 2, or 4 g betaine/100 g diet (no, 1, 2, and 4% betaine, respectively). Wild-type C57BL/6 J mice were fed AIN-93G diet (wild-type). Mice were sacrificed after 0, 7, or 14 weeks of the experimental diets. Atherosclerotic lesion area in the aortic sinus, levels of tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein (MCP)-1 in aorta and serum, serum lipids, and methylation status of TNF-alpha promoter in aorta were determined. RESULTS: Linear regression analysis showed that the higher dose of betaine was related to smaller atherosclerotic lesion area (beta = -11.834, P < 0.001). Compared with no-betaine mice after 14 weeks, mice receiving 1%, 2%, or 4% betaine had 10.8, 41, and 37% smaller lesion area, respectively. Betaine supplementation also reduced aortic expression of TNF-alpha in a dose-dependent way in four groups of apoE-deficient mice, and Pearson correlation revealed that atherosclerotic lesion area was positively associated with aortic TNF-alpha level (r = 0.777, P < 0.001). Although serum TNF-alpha levels were lower in betaine-supplemented mice than in no-betaine mice after fourteen weeks of treatment (P < 0.001), we did not observe a significant dosage effect (P = 0.11). However, methylation level of TNF-alpha promoter did not differ among groups at any time. In this study, apoE-deficient mice receiving betaine supplementation for 14 weeks had higher concentrations of serum total cholesterol (P < 0.01), LDL cholesterol (P < 0.05), and lower body weight (P < 0.05) than no-betaine mice. CONCLUSIONS: These data suggest that despite exacerbating hyperlipidemia in apoE-deficient mice, betaine may exert its anti-atherogenic effect by inhibiting aortic inflammatory response mediated by TNF-alpha.