We investigated the mechanisms leading to rapid death of corals when exposed to runoff and resuspended sediments, postulating that the killing was microbially mediated. Microsensor measurements were conducted in mesocosm experiments and in naturally accumulated sediment on corals. In organic-rich, but not in organic-poor sediment, pH and oxygen started to decrease as soon as the sediment accumulated on the coral. Organic-rich sediments caused tissue degradation within 1 d, whereas organic-poor sediments had no effect after 6 d. In the harmful organic-rich sediment, hydrogen sulfide concentrations were low initially but increased progressively because of the degradation of coral mucus and dead tissue. Dark incubations of corals showed that separate exposures to darkness, anoxia, and low pH did not cause mortality within 4 d. However, the combination of anoxia and low pH led to colony death within 24 h. When hydrogen sulfide was added after 12 h of anoxia and low pH, colonies died after an additional 3 h. We suggest that sedimentation kills corals through microbial processes triggered by the organic matter in the sediments, namely respiration and presumably fermentation and desulfurylation of products from tissue degradation. First, increased microbial respiration results in reduced O(2) and pH, initiating tissue degradation. Subsequently, the hydrogen sulfide formed by bacterial decomposition of coral tissue and mucus diffuses to the neighboring tissues, accelerating the spread of colony mortality. Our data suggest that the organic enrichment of coastal sediments is a key process in the degradation of coral reefs exposed to terrestrial runoff.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3386076PMC
http://dx.doi.org/10.1073/pnas.1100715109DOI Listing

Publication Analysis

Top Keywords

tissue degradation
12
hydrogen sulfide
12
anoxia low
12
corals exposed
8
degradation coral
8
corals
5
sediments
5
tissue
5
degradation
5
mechanisms damage
4

Similar Publications

Peripheral nerve injury repair has always been a research concern of scientists. At the tissue level, axonal regeneration has become a research spotlight in peripheral nerve repair. Through transplantation of autologous nerve grafts or other emerging biomaterials functional recovery after facial nerve injury is not ideal in clinical scenarios.

View Article and Find Full Text PDF

Ectopic Thyrotropin-Secreting Tumor in the Nasopharynx Causing Central Hyperthyroidism.

JCEM Case Rep

January 2025

Section of Endocrinology and Investigative Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College, London W12 ONN, UK.

We report a 31-year-old man with diarrhea and tachycardia. Diagnostic workup confirmed raised free thyroid hormones with unsuppressed thyroid stimulating hormone (TSH). Laboratory assay and medication interference were excluded.

View Article and Find Full Text PDF

Background: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive lethal malignancy with limited options for treatment and a 5-year survival rate of 11% in the United States. As for other types of tumors, such as colorectal cancer, aberrant lipid synthesis and reprogrammed lipid metabolism have been suggested to be associated with PDAC development and progression.

Aim: To identify the possible involvement of lipid metabolism in PDAC by analyzing in tumoral and non-tumoral tissues the expression level of the most relevant genes involved in the long-chain fatty acid (FA) import into cell.

View Article and Find Full Text PDF

Correlations of the expression of Cx43, SCF, p-cyclin E1 (Ser73), p-cyclin E1 (Thr77) and p-cyclin E1 (Thr395) in colon cancer tissues.

World J Gastrointest Oncol

January 2025

Department of Orthopaedics, Air Force Hospital of Eastern Theater, Anhui Medical University, Nanjing 230032, Jiangsu Province, China.

Background: Previous cellular studies have demonstrated that elevated expression of Cx43 promotes the degradation of cyclin E1 and inhibits cell proliferation through ubiquitination. Conversely, reduced expression results in a loss of this capacity to facilitate cyclin E degradation. The ubiquitination and degradation of cyclin E1 may be associated with phosphorylation at specific sites on the protein, with Cx43 potentially enhancing this process by facilitating the phosphorylation of these critical residues

Aim: To investigate the correlation between expression of Cx43, SKP1/Cullin1/F-box (SCF), p-cyclin E1 (ser73, thr77, thr395) and clinicopathological indexes in colon cancer.

View Article and Find Full Text PDF

Introduction: Oxidative stress is an important cause of acetaminophen (APAP)-induced liver injury (AILI). Sakuranetin (Sak) is an antitoxin from the cherry flavonoid plant with good antioxidant effects. However, whether sakuranetine has a protective effect on APAP-induced liver injury is not clear.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!