Reactive oxygen species accelerate humification process during iron mineral-amended sludge composting.

The production of hydroxyl radicals (OH) has been documented during composting. However, the effect of OH on composting efficiency remains unclear. Here, iron mineral supplemented thermophilic composting (imTC) is proposed and demonstrated for enhancing OH production and accelerating the maturation of composting. The results indicated that the maximum OH production of imTC was 1922.74 µmol·kg-1, which increased by 1.39 times than that of ordinary thermophilic composting (oTC). Importantly, the increase of OH could greatly enhance organic matter degradation and humic substances formation during imTC, resulting in shorting the maturity time by 25 %. Enrichment of laccase-producing bacteria resulted in higher laccase activity (31.85 U·g-1) in imTC compared with oTC (23.82 U·g-1), which may have contributed to the higher level of humification in imTC treatment. This work, for the first time, proposes a feasible strategy for improving composting efficiency through the regulation of OH production during aerobic composting.

Long-term use of fluoxetine accelerates bone loss through the disruption of sphingolipids metabolism in bone marrow adipose tissue.

Fluoxetine is a commonly prescribed antidepressant, and the mechanisms of increased bone fragility with its long-term use remain largely unknown. Here, we show that long-term administration of fluoxetine induces the disruption of sphingolipids metabolism in bone marrow adipose tissue (BMAT)through the inhibition of acid sphingomyelinase (ASM). Similarly, a significant reduction of the bone volume was observed in mice with ASM knockout (Smpd1-/-). In detail, inhibition of ASM by fluoxetine reduces the sphingosine-1-phosphate (S1P) level in bone marrow adipocytes, leading to the increase of receptor activator of nuclear factor-kappa-Β ligand (RANKL) secretion, a key regulator for the activation of osteoclastogenesis and bone loss, through the upregulation of cyclooxygenase-2 and its enzymatic product prostaglandin E2 (COX-2/PGE2). In contrast, overexpression of ASM by cisplatin normalizes fluoxetine-induced RANKL overproduction. Furthermore, we conducted a clinical trial with L-serine, a precursor of sphingolipids biosynthesis. The results show that oral supplementation of L-serine (250 mg//kg/d) prevents the acceleration of bone loss caused by long-term fluoxetine (12 months) in postmenopausal women with major depressive disorder (mean total hip bone mineral density reduction: -2.0% vs -1.1%, P = 0.006). Our study provides new insights and potential treatment strategy on the bone loss caused by long-term use of fluoxetine.