Journal of Advances in Biology & Biotechnology

Background: Rising ambient temperatures are progressively constraining the productivity, fertility and welfare of dairy and dual-purpose cattle (Bos taurus, Bos indicus) and water buffalo (Bubalus bubalis) across tropical, subtropical and increasingly temperate production systems. Beyond acute physiological disruption, accumulating evidence indicates that heat stress leaves molecular marks on the genome that persist within an individual and, in some cases, across generations.

Purpose: This critical narrative review synthesises evidence on the physiological, oxidative and epigenetic mechanisms linking heat stress to thermotolerance phenotypes in cattle and buffalo, with particular attention to the concept of an epigenetic "memory" of thermal experience and its purported transmission to offspring.

Methods: A structured web-based literature search of peer-reviewed veterinary, animal-science and molecular-biology sources was conducted, prioritising primary research and reviews published within the preceding decade, supplemented by foundational older work where conceptually necessary. Sources were appraised for methodological adequacy, species relevance and consistency of reported effects.

Principal Findings: Heat stress activates a conserved heat-shock response and disturbs the balance between reactive oxygen species and antioxidant defences, with buffalo generally showing a more pronounced oxidative and cellular stress phenotype than cattle at comparable thermal loads. Reactive oxygen species and heat-shock signalling converge on chromatin-modifying pathways, altering DNA methylation, histone marks and non-coding RNA profiles in somatic, gametic and embryonic tissue. In utero heat stress reproducibly reprogrammes the offspring epigenome, and several large observational cohorts in dairy cattle report reduced performance in daughters and granddaughters of heat-stressed dams, consistent with intergenerational, and in some analyses transgenerational, transmission. Direct mechanistic and buffalo-specific evidence for heritable epigenetic memory remains comparatively sparse, and findings on gamete- and oocyte-level methylation are inconsistent.

Conclusions and Implications: The weight of evidence supports oxidative stress and epigenetic reprogramming as biologically plausible, partially demonstrated mechanisms linking parental heat exposure to offspring phenotype, but causal, mechanistic proof of heritable epigenetic memory in ruminants remains incomplete, and is disproportionately derived from Bos taurus dairy systems rather than buffalo or indicine cattle.