Screening of Microorganisms for Biodegradation of Simazine Pollution (Obsolete Pesticide Azotop 50 WP)

The capability of environmental microorganisms to biodegrade simazine—an active substance of 2-chloro-s-triazine herbicides (pesticide waste since 2007)—was assessed. An enormous metabolic potential of microorganisms impels to explore the possibilities of using them as an alternative way for thermal and chemical methods of utilization. First, the biotope rich in microorganisms resistant to simazine was examined. Only the higher dose of simazine (100 mg/l) had an actual influence on quantity of bacteria and environmental fungi incubated on substrate with simazine. Most simazine-resistant bacteria populated activated sludge and biohumus (vermicompost); the biggest strain of resistant fungi was found in floral soil and risosphere soil of maize. Compost and biohumus were the sources of microorganisms which biodegraded simazine, though either of them was the dominant considering the quantity of simazine-resistant microorganisms. In both cases of periodic culture (microorganisms from biohumus and compost), nearly 100% of simazine (50 mg/l) was degraded (within 8 days). After the repeated enrichment culture with simazine, the rate of its degradation highly accelerated, and just after 24 h, the significant decrease of simazine (20% in compost and 80% in biohumus) was noted. Although a dozen attempts of isolating various strains responsible for biodegradation of simazine from compost and biohumus were performed, only the strain identified as Arthrobacter urefaciens (NC) was obtained, and it biodegraded simazine with almost 100% efficiency (within 4 days)

Leptin signalling genetic variants and insulin resistance in multiple sclerosis patients

Last decade provided multiple evidence that link disturbances in metabolic processes and energy metabolism with diseases of central nervous system and neurodegeneration. Initial phases of insulin resistance (IR) are present in natural course of multiple sclerosis (MS) and leptin was recognized as a player in MS pathophysiology and moreover cognitive decline. We aimed to investigate association of genetic variants in leptin (LEP) rs7799039, its receptor LEPR rs1137101 and proliferator-activated receptor gamma co-activator 1-alpha (PGCA1A) rs8192678 with IR parameters (HOMA-IR index, area under the curve for insulin and glucose, Cederholm insulin sensitivity index (ISIced), the insulinogenic index in the first 30 min of oral glucose tolerance test (OGTT) in patients with MS. Seventy eight relapsing-remitting patients in clinical remission, free of corticosteroids for at least three months, were included in the study. None of the 3 variants’ genotypes were associated with HOMA-IR index, area under the curve for insulin and glucose and the insulinogenic index in the first 30 min of OGTT. PGC1A variant was significantly associated with ISIced (Kruskal-Wallis ANOVA, p = 0.04). Leptin gene variant was significantly associated with impaired GT (p=0.029 adjusted for gender and other two variants). None of the variant showed association with IR. In conclusion, we found that genetic variants in leptin signalling pathway affect glucose tolerance and insulin sensitivity in patients with MS. As both, leptin and PGC1A have role in preventing neuronal death and reducing oxidative stress neuronal damage current results favour further investigation toward preserving cognitive status and neuroprotection in MS.17th World Congress on Controversies in Neurology; March 23-25, Dubrovnik, Croatia, 2023