Histopathology of respiratory organs of certain air-breathing fishes of India

Abstract

Air-breathing fishes have evolved bimodal respiratory mechanisms for exploitation of water (through gills and highly vascularized skin) as well as atmospheric air (through aerial respiratory organs, ABO). Mucous cells in these respiratory organs of variously stressed fishes exhibit periodic fluctuations in their density and staining properties. The main types of damage in the gills include congestion of blood capillaries (BLCs), periodic lifting and sloughing of respiratory epithelia of the secondary lamellae causing haemorrhage, extensive fusion of secondary lamellae and hyperplasia of the respiratory epithelia due to uncontrolled regeneration leading to asphyxiation, altered excretion, and death of the fish. Haemolysis has also been observed following lead exposure. The damage in the ABO of Heteropneustes fossilis includes sloughing of the epithelial cells, leading to haemorrhage causing decreased red blood corpuscles density and degeneration of the secondary gill lamellae with reduced respiratory area. Subsequent hyperplasia of the respiratory epithelia and fusion of gill lamellae increase the respiratory barrier distance. The BLCs often bulge out and protrude into the lumen, bringing blood nearer to air. The ladderlike pillar cell (PLC)-BLC components of the gill lamellae frequently collapse. Damage to the ABO of Channa striata is less severe. Often haemorrhaging due to bursting of extensively stretched BLCs causes aerial respiratory failure. Chloride cells of the ABOs also show hyperplasia. While the highly mucogenic epidermis of C. striata shows less damage, the epidermis of Clarias batrachus and H. fossilis shows severe wear and tear, sloughing, and haemorrhage. Side-by-side regeneration continues, causing altered histomorphology of the epidermis. The different gland cells also show periodic fluctuations in their density and staining. The dermis also shows severe damage with loosening of their connective tissue fibres. These fibres give stronger reactions for sulfated mucin that not only retain additional water molecules for continuance of skin breathing, but also bind the toxic ambient pollutants.

Effect of Single Superphosphate Fertilizer on Survival and Respiratory Dynamics of Nile Tilapia, <I>Oreochromis Niloticus</I> (Actinopterygii: Perciformes: Cichlidae)

“…Respiratory irregularities noticed in exposed fish could have been caused by mucous precipitation on the gill epithelia in response to the toxicant which resulted in abnormal behaviour as earlier documented by Banerjee (2007). In addition, reduction in the activity levels of respiratory enzymes such as LDH and ADH and the depletion in the level of consumed oxygen could all have contributed to the observed behaviour and eventual mortality.…”

“…The sensitivity of Oreochromis niloticus exposed to SPF resulted in the degeneration of the gill lamellae, which according to Omoregie and Ufodike (1991), Banerjee and Chandra (2005), and Banerjee (2007) would lead to branchial malfunctioning. Results from this investigation have revealed that degenerated gill lamellae have far-reaching consequences for oxygen uptake by the fish and therefore homeostasis in the fish system.…”

“…Banerjee (2007) noted that congestion of blood capillaries, periodic lifting and sloughing of respiratory epithelia of the secondary lamellae and haemorrhages are the major main damages observed on fish gills in polluted water bodies. This author also noted the extensive fusion of secondary lamellae and hyperplasia of the respiratory epithelia due to uncontrolled regeneration are the major causes leading to asphyxiation, and eventually death of the fish if exposure is prolonged excessively.…”

Study of sodium arsenite induced biochemical changes on certain biomolecules of the freshwater catfish Clarias batrachus

“…The main reason for protein decrease in these boundary tissues might be due to excessive synthesis followed by sloughing of the slime (made up of glycoprotein) induced by the arsenic stress. For inducing increased secretion of slime in the skin and gills the concentration of RNA also increases (Banerjee, 2007). The other probable reason for the loss of proteins might be due to rejection of damaged cellular components of the skin and gills rendered by the contact stress of different toxicants (Parashar & Banerjee, 2002;Hemalatha & Banerjee, 2003;Chandra & Banerjee, 2005;Devi & Banerjee, 2006;Banerjee, 2007), including an arsenic salt (Singh & Banerjee, 2008).…”

“…For inducing increased secretion of slime in the skin and gills the concentration of RNA also increases (Banerjee, 2007). The other probable reason for the loss of proteins might be due to rejection of damaged cellular components of the skin and gills rendered by the contact stress of different toxicants (Parashar & Banerjee, 2002;Hemalatha & Banerjee, 2003;Chandra & Banerjee, 2005;Devi & Banerjee, 2006;Banerjee, 2007), including an arsenic salt (Singh & Banerjee, 2008). Sloughing of damaged cells from the surface of the skin also causes decreased amount of DNA in the skin exposed to the arsenic solution for prolonged period (Table 1).…”