Acute Exposure to Two Biocides Causes Morphological and Molecular Changes in the Gill Ciliary Epithelium of the Invasive Golden Mussel Limnoperna fortunei (Dunker, 1857)

SIMPLE SUMMARY: Limnoperna fortunei, known as the golden mussel, is an invasive bivalve in South America responsible for economic damages in hydroelectric plants due to its ability to attach and grow on the walls of water pipes and tubes. Chemical compounds are often used to control golden mussel infestations in water systems. Here, we investigated the effects of two biocides—MXD-100 ™ and sodium dichloroisocyanurate (NaDCC)—through the assessment of morphological and gene-expression alterations in the gills. Both biocides were able to modulate the expression of defensive genes and morphological changes. Yet, it seems that NaDCC needs continuous exposure to control golden mussel infestation, whereas MXD-100™ can inflict severe damage to the mussels in as little as 24 h. Our results can be used to enhance control strategies for managing mussel growth in water systems, simultaneously reducing the environmental impact associated with costly and harmful chemical releases. ABSTRACT: Limnoperna fortunei, the golden mussel, is a bivalve mollusk considered an invader in South America. This species is responsible for ecological and economic damages due to its voluminous fouling capability. Chemical biocides such as MXD-100™ and sodium dichloroisocyanurate (NaDCC) are often used to control L. fortunei infestations in hydraulic systems. Thus, we proposed to investigate the effects of different periods (24, 48 and 72 h) of exposure to MXD-100™ (0.56 mg L(−1)) and NaDCC (1.5 mg L(−1)) on the gills of L. fortunei through morphological and molecular analyses. NaDCC promoted progressive morphological changes during the analyzed periods and only an upregulation of SOD and HSP70 expression during the first 24 h of exposure. MXD-100™ led to severe morphological changes from the first period of exposure, in addition to an upregulation of SOD, CAT, HSP70 and CYP expression during the first 24 h. In contrast, MXD-100™ led to a downregulation of CAT transcription between 24 and 48 h. In static conditions, NaDCC causes lethal damage after 72 h of exposure, and that exposure needs to be continuous to achieve the control of the species. Meanwhile, the MXD-100™ treatment presented several effects during the first 24 h, showing acute toxicity in a shorter period of time.