Aluminium Toxicity in Fish – Histopathological Findings

Aluminium (Al) is a widely distributed metal, concentrations of which can vary in aquatic ecosystems due to different anthropogenic activities; this is especially true in freshwater. Aluminium has no functional use in cellular processes and its presence in high concentrations results in mortality. Sublethal concentrations may disturb production cycles, affecting growth, and in salmonids, subsequent tolerance to seawater.

Inorganic monomeric positively charged Al species are considered the most toxic Al forms, especially in acid waters. Episodic acidification resulting in increased inorganic aluminium is known to impact anadromous salmonids and has been identified as a cause of Atlantic salmon population decline. For instance, several studies have shown that Atlantic salmon smolts are the most sensitive of the salmon life-stages to ion regulatory disturbance resulting from acid/Al exposure. Such exposure may cause nephropathy and subsequent death.

Gills are the primary target of Al toxicity but other organs such as liver, kidney, muscle, brain and heart can also be affected in chronic exposure. Early changes in renal tubules include hydropic swelling, progressing to tubular necrosis, and renal insufficiency.

Deposition of aluminium in gills leads to chloride cell necrosis or at lower levels, to inhibition of the enzymes carbonic anhydrase and/or gill NA+, K+ – ATPase (NKA), required for seawater tolerance. Such changes impair osmoregulatory capacity and cause physiological stress due to disruption of gas and ion transport, altered blood chemistry and hormonal imbalance.

Impairment of gill respiratory function is associated with histopathological changes such as thickening of the lamellar epithelium, lamellar fusion and hyperplasia of the filamental epithelium; in total these changes increase blood-water diffusion distance and reduce surface area for gas exchange. 

Along with Al accumulation in gills, accumulation in bone/cartilage can also be observed by means of Al-specific histochemistry.

Table 1. Comparison of optimal Aluminium concentration range.


Figure 1. H&E. Kidney. S. salar. Smolt. Early hydropic degeneration of tubular epithelium. A few tubules have early casts.
Figure 2. H&E. Kidney. S. salar. Smolt. Severe hydropic degeneration of tubular epithelium.
Figure 3. H&E. Kidney. Atlantic salmon fingerling with early hydropic degeneration of tubular epithelium.
Figure 4. H&E. Kidney. Atlantic salmon fingerling exposed to high Al concentration with degeneration and necrosis of tubular epithelium.
Figure 5. Histochemistry. Gills. Atlantic salmon smolt branchial arch cartilage/bone with positive reaction to Al-specific histochemistry stain (intense red colour).
Figure 6. Histochemistry. Gills. Fingerling lamellae cartilage/bone positive to Al-specific histochemistry stain (intense red colour).
Figure 7. Immunohistochemistry. Liver S. salar. Fingerling. Experimental intoxication with positive expression of specific protein related to metal intoxication, 72 hours post initial exposure.
Figure 8. Immunohistochemistry. Kidney. S. salar. Fingerling. Experimental intoxication with positive expression of specific protein related to metal intoxication, 72 hours post initial exposure.


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