Mitochondria-rich cells changes induced by nitrite exposure in tambaqui (Colossoma macropomum Cuvier, 1818).

Oscar T.F Da Costa,Wallice P Duncan,Juliana L.V Lameiras,Cleverson A Ramos,Marisa N Fernandes

doi:10.1590/0001-3765201720160648

Abstract

The gill mitochondria-rich cells of the juvenile Amazonian fish Colossoma macropomum were analyzed using light and scanning and transmission electron microscopy after 96 h exposure to 0.04 and 0.2 mM nitrite. Although the number of mitochondria-rich cells decreased significantly in the lamellar epithelium, no decrease was found in the interlamellar region of the gill filament. Nitrite exposure caused significant reduction on the apical surface area of individual mitochondria-rich cells (p < 0.05), with a resulting reduction of the fractional area of these cells in both the lamellar and filament epithelium. Swelling of endoplasmic reticulum cisternae, nuclear envelope and mitochondria were the main changes found in the mitochondria-rich cells. Cristae lysis and matrix vacuolization characterized the mitochondrial changes. The overall ultrastructural changes indicated cellular functional disruption caused by exposure to nitrite. The changes observed in the gill indicate that the cellular structures involved in the process of energy production become severely damaged by exposure to nitrite indicating irreversible damage conducting to cell death.

Highlights

Nitrite (NO2-) is an intermediate product of bacterial ammonia decomposition that occurs naturally in ecosystems
The morphology of gill filaments and lamellae of C. macropomum (Figure 1a-c) is similar to that described for other teleost species
The secondary lamellae were regularly spaced on both sides of the gill filaments and consisted of two epithelial layers of cells separated by rows of pillar cells interspersed with blood spaces

Summary

Introduction

Nitrite (NO2-) is an intermediate product of bacterial ammonia decomposition that occurs naturally in ecosystems. Low environmental levels are maintained as a result of balanced bacteriadriven nitrification and denitrification processes (Lewis Jr and Morris 1986, Jensen 2003). NO2- is beneficial for fish as an exogenous reservoir for nitric oxide, which is a key signaling molecule in cardiovascular regulation (Hansen and Jensen 2010, Jensen and Hansen 2011). High concentrations are related to mass fish mortality (Svobodová et al 2005). Some environmental conditions such as temperature and high levels of organic matter favor the occasional development of NO2- in the Amazonian environment and in fish culture systems. The active mechanism for NO2- uptake by the gill mitochondria-rich cells (MRCs) and its possible toxic effect on these cells were previously discussed (Jensen 2003, Williams and Eddy 1986, Gaino et al 1984)

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