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Abstract

Atmospheric soot loadings from nuclear weapon detonation would cause disruptions to the Earth’s climate, limiting terrestrial and aquatic food production. Here, we use climate, crop and fishery models to estimate the impacts arising from six scenarios of stratospheric soot injection, predicting the total food calories available in each nation post-war after stored food is consumed. In quantifying impacts away from target areas, we demonstrate that soot injections larger than 5 Tg would lead to mass food shortages, and livestock and aquatic food production would be unable to compensate for reduced crop output, in almost all countries. Adaptation measures such as food waste reduction would have limited impact on increasing available calories. We estimate more than 2 billion people could die from nuclear war between India and Pakistan, and more than 5 billion could die from a war between the United States and Russia—underlining the importance of global cooperation in preventing nuclear war.

Abstract

There has been an alarming trend toward earlier puberty in girls, suggesting the influence of an environmental factor(s). As the reactivation of the reproductive axis during puberty is thought to be mediated by the hypothalamic neuropeptides kisspeptin and gonadotropin-releasing hormone (GnRH), we asked whether an environmental compound might activate the kisspeptin (KISS1R) or GnRH receptor (GnRHR). We used GnRHR or KISS1R-expressing HEK293 cells to screen the Tox21 10K compound library, a compendium of pharmaceuticals and environmental compounds, for GnRHR and KISS1R activation. Agonists were identified using Ca2+ flux and phosphorylated extracellularly regulated kinase (p-ERK) detection assays. Follow-up studies included measurement of genes known to be upregulated upon receptor activation using relevant murine or human cell lines and molecular docking simulation. Musk ambrette was identified as a KISS1R agonist, and treatment with musk ambrette led to increased expression of Gnrh1 in murine and human hypothalamic cells and expansion of GnRH neuronal area in developing zebrafish larvae. Molecular docking demonstrated that musk ambrette interacts with the His309, Gln122, and Gln123 residues of the KISS1R. A group of cholinergic agonists with structures similar to methacholine was identified as GnRHR agonists. When applied to murine gonadotrope cells, these agonists upregulated Fos, Jun, and/or Egr1. Molecular docking revealed a potential interaction between GnRHR and 5 agonists, with Asn305 constituting the most conservative GnRHR binding site. In summary, using a Tox21 10K compound library screen combined with cellular, molecular, and structural biology techniques, we have identified novel environmental agents that may activate the human KISS1R or GnRHR.

Editor’s summary

Only a few of the many volcanism-driven hyperthermals during the Phanerozoic caused mass extinctions, and none of them approached the level of global species loss seen at the end of the Permian. Why was the end-Permian so different? Sun et al. found that a combination of extreme El Niño events and mean state warming led to deforestation, reef demise, and a plankton crisis, all of which resulted in a positive feedback cycle that led to an even warmer mean climate and still stronger El Niño events. —Jesse Smith

Abstract

The ultimate driver of the end-Permian mass extinction is a topic of much debate. Here, we used a multiproxy and paleoclimate modeling approach to establish a unifying theory elucidating the heightened susceptibility of the Pangean world to the prolonged and intensified El Niño events leading to an extinction state. As atmospheric partial pressure of carbon dioxide doubled from about 410 to about 860 ppm (parts per million) in the latest Permian, the meridional overturning circulation collapsed, the Hadley cell contracted, and El Niños intensified. The resultant deforestation, reef demise, and plankton crisis marked the start of a cascading environmental disaster. Reduced carbon sequestration initiated positive feedback, producing a warmer hothouse and, consequently, stronger El Niños. The compounding effects of elevated climate variability and mean state warming led to catastrophic but diachronous terrestrial and marine losses.