Metal X‐ray microanalysis in the olfactory system of rainbow trout exposed to low level of copper

Abstract

Summary— It has recently been shown that a chronic copper exposure induces specific degeneration of olfactory receptor cells in rainbow trout; however, the exact mechanism of action of the metal is not yet known. Using X‐ray microanalysis in transmission electron microscopy, we have studied the distribution of metal in the olfactory system of fish exposed for 15, 30 and 60 days to 20 μg/l of copper. This was done in order to determine if it was accumulated in receptor cells and transported into the central nervous system via the olfactory nerve. No copper accumulation was detected either in the olfactory epithelium, in the olfactory nerve or in the olfactory bulb. The heavy metal was exclusively found within melanosomes of melanophores located in the lamina propria. After 60 days of exposure, the copper content in melanosomes was about two‐fold higher than that in controls. As far as some morphological recovery took place in the olfactory organ during the metal exposure, which lets us suppose that some detoxication mechanism occurs, it could be suggested that melanophores might be somehow involved in such a mechanism.

Effect of Acute Copper Sulfate Exposure on Olfactory Responses to Amino Acids and Pheromones in Goldfish (Carassius auratus)

“…Structural recovery is delayed, with the epithelium recovering only after 14 weeks (30). Nevertheless, copper does not accumulate in the olfactory system (31).…”

Cadmium disrupts behavioural and physiological responses to alarm substance in juvenile rainbow trout (Oncorhynchus mykiss)

“…Several studies have illustrated the sensitivity of olfaction to toxicants, including cadmium (Brown et al, 1982;Stromberg et al, 1983), copper (Hara et al, 1976;Brown et al, 1982;Rehnberg and Schreck, 1986;Julliard et al, 1995;Hansen et al, 1999), diazinon (Moore and Waring, 1996) and mercury (Hara et al, 1976;Brown et al, 1982;Rehnberg and Schreck, 1986). It has recently become apparent that olfactory disruption by sublethal toxicant exposure may consequently disturb olfaction-mediated predator avoidance behaviours of fish.…”

Responses of wild fishes to alarm chemicals in pristine and metal-contaminated lakes

“…It is suspected that free metal cations present in metal-contaminated lakes disrupt olfaction by damaging olfactory epithelium, leading to an impairment of olfactory function (Klima and Applehans 1990;Hansen et al 1999b;Beyers and Farmer 2001;Scott et al 2003). However, some research suggests that fish exposed to elevated concentrations of aqueous metals can maintain chemosensory function in the long term through physiological adaptation and the development of tolerance with increasing exposure time (Hara 1994;Julliard et al 1995;Beyers and Farmer 2001). Beyers and Farmer (2001) reported that an initial loss of olfactory ability occurred during the first 24 h of exposure to a range of copper concentrations (<10 to 266 µg/L), but within days, olfactory ability recovered in fish held at concentrations <66 µg/L owing to the induction of protective mechanisms such as increased mucus production, the induction of detoxifying mechanisms, or metal sequestration by melanophores.…”

“…Receptor cells that are sensitive to alarm cues are located in the olfactory epithelium (Klima and Applehans 1990) and are directly and continuously in contact with the aquatic environment (Julliard et al 1995). But what happens when this olfactory epithelium is exposed to chemical pollution such as aqueous metals?…”

“…But what happens when this olfactory epithelium is exposed to chemical pollution such as aqueous metals? Laboratory studies have shown that aqueous metal contamination affects freshwater fishes and their ability to perceive chemical signals (Julliard et al 1995;Scott et al 2003). Hansen et al (1999a) reported that chinook salmon (Oncorhynchus tshawytscha (Walbaum in Artedi, 1792)) pre-exposed to 2 µg Cu/L failed to avoid potentially toxic Cu concentrations (>44 µg/L) owing to Cu-induced damage to olfactory epithelium during the pre-exposure period.…”